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Interstitial Gingivitis 




Eugene S. Talbot, M. S., D. 1). S., M. 1)., LL. 1). 

Late Professor of Stomatology, Woman's Medical School, Northwestern University 
Late Lecturer on Stomatology, Rush Medical College, University of Chicago; Fellow 
of The Chicago Academy of Medicine; Fellowship Member of the New York State 
Dental Society, 1908; Secretary of Section on Stomatology of the American 
Medical Association; Vice-President American Medical Association, 1905; 
Member VII International Medical Congress. 1881, London; Honorary Presi- 
dent X International Medical Congress, 1890. Berlin; Honorary President 
XII International Medical Congress, 1897, Moscow; Corresponding 
Member, Budapest Royal Society' of Physicians; Honorary President 
International Association of Stomatology. 1907, Paris; Member First 
French Congress of Stomatology, 1907, Paris; Honorary Secretary- 
Pan-American Medical Congress, 1901, Havana; Honorary Member 
Odontologischen Gesellschaft, Berlin; Honorary Member 
Association Generale des Dentistes de France. Paris: Honor- 
ary Member Sociedad Odontological Espanola, Madrid; 
Corresponding Member Dansk-Tandlaegeforening. 1901; 
Honorary Member Stomatology Society of Hungary; 
Corresponding Member of the Italian Stomatological 
Federation, 1910; Member Chicago Academy of 
Sciences; Member American Association for the 
Advancement of Science; Charter Member 
American Institute of Criminal Law and 
Criminology; Member of the Author's 
Club, London. 
Author of the following books: "The Irregularities of the Teeth and their Treatment;'' 
"Chart of Typical Forms of Constitutional Irregularities of the Teeth;" The 
Etiology of Osseous Deformities of the Head, Face, Jaws and Teeth;" 
"Degeneracy: Its Signs. Causes and Results;" "Developmental 
Pathology: A Study in Degenerative Evolution," etc., etc. 






IT 3 




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In this book the etiology, pathology and treatment of peri- 
dental disease have been worked out by actual research which 
covered a period of thirty-five years. Up to the present time 
teachers and practitioners have taught that disease of the gums 
and alveolar process was of a pyorrhceic or infectious nature. 
All etiologic experiments and treatment are made from this 
basis. The tendency at the present time is to study diseases of 
the body from a bacteriological view point. It is now known 
that many different tissues and organs of the body undergo 
physiologic and chemic changes which are often due to irrita- 
tions setting up inflammation and may later under certain con- 
ditions become infected by bacteria. Inflammations of the 
mucous membranes due to acid states and burns are of this 
nature. It has been the aim of the author to classify the 
inflammations due to infections and those due to chemic 
changes and local and constitutional irritations. The diseases 
of the alveolar process due to infections are usually of systemic 
origin and develop symptoms in other parts of the body such as 
tuberculosis, typhoid fever, anthrax, actinomycosis, etc., and 
are rarely referred to the specialist for treatment. The pa- 
tients referred to the specialists are those with inflammations 
of the gums, mucous membrane and alveolar process due to 
irritations and which may or may not later become infected by 

The author has observed that every vertebrate having two 
sets of teeth during life may possess an inflammatory condition 
of the alveolar process to a greater or less extent after the first 
set of teeth has developed depending upon environment and 
the condition of the system. 

The pyorrhceic stage which may develop later is observed 
in only a very small per cent of patients. Happily, to a certain 

extent, the profession has come to realize the importance of the 
two periods and the teaching of the pathology and bacteriology 
of the disease is much simplified and better understood. 

The great law of medical science, that to know the cause is 
half the treatment, is as applicable to diseases of the mouth as 
to any other specialty of medicine, and is as applicable to dental 
problems as to those of biology generally. Treatment of any 
disease without knowledge of its pathology is practically a 

While much has been written upon the pyorrhceic stage of 
interstitial gingivitis and its treatment, during the past two 
decades, no new principle has been advanced whereby the parts 
can be restored to a healthy condition, or whereby the disease 
can be prevented. The disease is admittedly on the increase. 
This seems at first sight to indicate that d ental prophyl axis and 
treatment, so far as this disease is concerned, are failures. 

Nearly three decades ago I felt and expressed the necessity 
for more extended study (Dental Cosmos, 1886, page 689) of 
the clinical aspects and etiology of this disease. Even during 
apparently diverse and separated studies, such as those related 
to dental and maxillary irregularities and degeneracy, the ne- 
cessity for this has forced itself still further upon me. In the 
present study, the disease has, of necessity, been considered 
from the broad standpoint of general pathology. In all in- 
stances where possible personal elements of error are present, 
these have been eliminated by having researches made by more 
than one observer. 

The attempt has been made to summarize all researches on 
the subject. So much have opinions been intermingled that it is 
possible that proper credit for priority has unintentionally not 
been given. 

The author is under obligation to the following scientists for 
their kind assistance : Dr. Ludwig Hektoen, Pathologist, Bush 
Medical College; Dr. Jerome H. Salisbury, Chemist, Bush 
Medical College ; Dr. W. A. Evans, Pathologist, Columbus Med- 
ical Laboratory, Professor of Pathology, Chicago College of 
Physicians and Surgeons and Milwaukee Medical College; Dr. 
J. A. Wesener, Chemist, Columbus Medical Laboratory, Profes- 

sor of Chemistry, Chicago College of Physicians and Surgeons ; 
Dr. Vida A. Latham, Pathologist, Northwestern Uinversity, 
Woman's Medical School; Dr. Maximilian Herzog, Pathologist, 
Chicago Polyclinic Hospital; Professor Theo. A. Edwin Klebs 
and Dr. Robert F. Zeit, Pathologists, and Dr. W. L. Baum, 
Professor of Diseases of the Skin, Post-Graduate Medical 
School, Chicago; Dr. G. V. I. Brown, Professor of Oral Sur- 
gery, Dental Department, Milwaukee Medical College; Dr. 
Frederick Noyes, Histologist, Dental Department, Northwest- 
ern University; Dr. J. G. Kiernan, and to Blomgren Bros. & 
Co. for electrotypes, etc. 

31 North State Street, Chicago. 





























History 1 

Introduction 13 

Transitory Structures : The Jaws 19 

Transitory Structures : The Alveolar Process ... 24 

The Alveolar Process Under the Microscope .... 35 
The Gums, Periosteum, Mucous and Peridental 

Membranes Under the Microscope 38 

Inorganic Salts and Interstitial Gingivitis 73 

Theories of Interstitial Gingivitis 84 

Uric Acid and Interstitial Gingivitis 87 

Heredity and Environment in Interstitial Gingi- 
vitis 95 

Degenerate Tissues in Interstitial Gingivitis .... 100 
Bacteriologic Researches in Interstitial Gingi- 
vitis 104 

Interstitial Gingivitis 112 

Researches on Animals in Interstitial Gingivitis . 125 

Researches on Human in Interstitial Gingivitis. 156 

Researches on Human in Pericementitis 175 

Local Causes of Interstitial Gingivitis 182 

Constitutional Causes of Interstitial Gingivitis. 194 

Climatic Influences in Interstitial Gingivitis .... 211 

Scurvy in Interstitial Gingivitis 218 

Toxins Producing Trophic Changes 223 

Autointoxication in Interstitial Gingivitis 235 

Urinary Signs of Autointoxication 247 

Arteriosclerosis, Endarteritis Obliterans and 

Nerve End Degeneration 261 

Absorption of the Alveolar Process and Calcic 

Deposits Upon the Roots of the Teeth 275 

Pyorrhoea Alveolaris 285 

Constitutional Effects of Pyorrhoea Alveolaris. . 295 

Treatment 310 

Bibliography 330 

Index 335 



Inflammation of the peridental membrane and alveolar pro- 
cess is probably coeval with man. Some of the skulls found 
earliest in the cave-dwelling- period exhibit evidences of its 
presence. In some of these, careful observation has shown de- 
posits encroaching upon the roots of the teeth and resultant ab- 
sorption of the alveolar process. 

In the Swiss lake-dwellings and in the earlier Irish cran- 
noges of like construction and situation, skulls are found, which 
exhibit deposits of tartar, inflammation of the peridental mem- 
brane and absorption of the alveolar process. These skulls were 
those of primitive races in whom disease of the jaws and teeth is 
supposed to be absent or infrequent. In the skulls of the peo- 
ples exhibiting the highest civilization at the earliest period — 
those of the Accadians and Egyptians — similar inflammatory 
conditions are to be found. This, however, was to have been 
expected, to judge from the dental directions left among the 
medical records of these peoples. The Greeks, Syrians, Arab- 
ians, Dravidians and Aryans of India and the early Burmese 
all suffered from this disorder. In the museum at Constan- 
tinople are the skulls of soldiers who fought at a battle 328 
B. C. One of these skulls has the anterior alveolar process 
entirely absorbed away. The roots of the right central, the 
right lateral and the left central incisors are exposed. 

Inflammation of the peridental membranes and alveolar proc- 
ess, it will be evident, is, therefore, not a modern disease ; not a 
disease confined either to civilized or primitive races, but one 
which attacked man early in his evolution. Like most diseases 
it has been chiefly discussed and analyzed during the past two 


In 1740 H. A. Fauchard 1 (while recognizing the disease in 
all its essential features and describing its principal symptoms) 
advanced no theory as to its origin. 

In 1778 M. Jourdain 2 advanced the opinion that the disease 
was of scorbutic origin. 

In 1821 L. Kaecker 3 discussed the disorder in an essay on 
the devastations of the gums and alveolar processes. 

In 1822 M. Joirac 4 (in a discussion of the disease), while 
advancing no theory as to its origin, called it "pyorrhoea inter- 
alveolo-dentaire. ' ' 

In 1860 Marshall de Calve 5 advanced the opinion that the 
disorder was of hereditary origin. 

In 1867 Magitot, discussing the disorder, advanced the 
opinion that the gum, being in all cases only attacked subse- 
quently, is not the original seat of the lesion. In his opinion 
systemic disorders like gout, rheumatism, albuminuria, diabetes 
and anaemia had an influence. 

Bonwill 6 during the same year expressed the opinion that 
the disorder was due to thinness of the alveolar process between 
the teeth, thus depriving the peridental membrane and gum 
tissue of proper support. The want of proper articulation of 
the teeth also exerted an influence. 

In 1870 Brown ascribed the disorder to serumal calculus. 

In 1875 John T. Riggs, after whom the disorder is frequently 
called, entitled it (in a paper read before the American 
Academy of Dental Surgery) suppurative inflammation of the 
gums and absorption of the gums and alveolar process. 

During the same year Scheff 7 of Vienna entitled the disorder 
periostitis dentalis. He was of the opinion that it originated 
from external irritation through mechanical, thermic and chemic 
changes. The real origin of the disorder was, in his opinion, 
very often obscure. He doubted, however, the influence of 
rheumatism. v ' ; 

1 Independent Dental Journal, 1875. 

1 Philadelphia Journal of Medical and Physical Science, 1821. 

'International Dental Journal, Vol. XIII. 

1 Journal of the American Medical Association. 

1 Journal of the American Medical Association. 

1 Dental Cosmos, Vol. XXIV. 

' Wiener Med. Presse, Vol. XVI. 

In 1876 Sirletti 8 (in a discussion of the pathology of the 
disorder, which he called alveolo-dental periostitis) regarded it 
as due to constitutional conditions, like rheumatism, scrofula, 
syphilis, etc., with local causes as exciting factors. 

In 1877 Rehwinkle, 9 in a paper on pyorrhoea alveolaris, after 
citing from Albright (of Berlin) the claim that the disorder 
was due to uncleanliness, mercury and the suppression of habit- 
ual secretions, expressed the opinion that acquired and inherited 
constitutional defect often played an important part as etiologic 
factors. He was also of opinion that mercury exerted an influ- 
ence in its causation. Salivary deposits were, in his opinion, 
without influence. 

Clowes 10 was of opinion in 1879 that the general cause was 
lack of nutrition in the parts. The use of wedges often excited 
the disorder. 

C. J. Essig, 11 in 1880, expressed the opinion that its predis- 
posing causes were unknown, that it occurred as a rule in healthy 
persons, and that irregular and crowded teeth acted as an excit- 
ing cause. 

In another paper during the same year G. A. Mills 12 ex- 
pressed the opinion that the disorder was of systemic origin. 
Various mental and physical influences aided its progress, such 
as nervous exhaustion and bodily and mental overwork. In his 
opinion it frequently occurred in children and adolescents from 
eruptive fevers. The deposit was only a local manifestation of 
the disorder. 

In 1881 N. S. Niles 13 expressed the opinion that constitu- 
tional conditions were, as a rule, without influence, and that local 
irritating deposits were the cause in twenty-five per cent of the 
cases coming under his observation. He was of opinion also 
that the amount of lime salts taken into the system in drinking 
water exerted an influence. A calcic and phosphatic diathesis 
had an influence in the production of the disorder. 

Gazzetta Modica di Roma. 1876. 

T>ntal Cosmos. Vol. XIX. 
'Ibid., Vol. XXI. 

Dental Cosmos, Vol. XXI. 
1 Ibid., Vol. XXTTI. 
1 Ibid.. Vol. XXIV. 


In 1881 (when there seemed to have been many contributions 
to the literature of the subject) Atkinson 14 expressed the opinion 
that nervous debility or original defect in innervation exerted an 
influence in the production of the disorder. The deposits of 
tartar were a secondary consequence. In the course of his paper 
he cited the opinion of Hamilton Cartwright that Riggs 's disease 
commenced in an unhealthy condition of the gums with a sec- 
ondary deposit of tartar. 

In a paper read before the Dental Section of the Inter- 
national Medical Congress, Walker 15 claimed that the starting 
point of the disease was subacute inflammation passing into the 
depths of the alveolar process adjacent to the inflamed gum. In 
the discussion of this paper, Archovy and Joseph Izklai, of 
Buda Pesth, ascribed the disorder to minute organisms. Oakley 
Coles thought that systemic states were the predisposing factors, 
while minute organisms exerted an exciting influence. 

In 1882, L. C. Ingersoll 16 regarded sanguinary calculus as a 
manifestation of the disorder, and distinguished it from salivary 

Malasses and Gallippe, 17 in 1884, expressed the opinion that 
the disorder was of microbic origin. 

In 1885, A. 0. Eawls 18 expressed the opinion that the causes 
were environment with morbid factors, such as malaria, exces- 
sive sodium, etc., chloride and mercury. 

In 1886, Reese 19 expressed the opinion that the disorder had 
its source in the uric acid diathesis resultant on abuse of alcohol. 

During the same year, J. D. Patterson 20 expressed the opin- 
ion that the disorder was of catarrhal origin. Later, in 1886, J. 
N. Farrar 21 regarded the disorder as a combined result of sys- 
temic tendencies and local irritants. There was a peculiar con- 
dition of the system associated with hypersecretion laden with 
increased earthly deposits. 

11 Dental Cosmos, Vol. XXIV. 

15 Transactions of the International Medical Congress, 1881. 

10 Dental Cosmos, Vol. XXV. 

« Ibid., Vol. XXVI. 

18 Ibid., Vol. XXVII. 

19 Independent Practitioner, Vol. VI. 

20 Dental Cosmos, Vol. XXI. 

21 Independent Practitioner, Vol. VII. 

A. R. Starr later also expressed the same opinion. He, how- 
ever, was unable to determine the local irritation factor, but 
regarded it as the same as that which causes exostosis of the 
cementum. He had found most cases in the upper jaws. 

Black 22 designated the disorder phagadenic pericementitis. 
It was a specific infection of an inflammatory character, having 
its origin in the gingiva, and was accompanied with destruction 
of the peridental membrane and alveolar walls. 

E. S. Talbot 23 during the same year regarded the disorder as 
a local one, due to both local and constitutional causes. The 
disorder began with simple inflammation of the gums, which 
afterward became chronic. 

He laid particular stress upon the anatomy, physiology and 
pathology of the parts involved, there being no other struc- 
tures in the human body like them, hence their easy suscepti- 
bility to disease. 

We may consider, then, as predisposing and exciting causes 
a perverted condition of the secretions, low vitality of patient or 
tissues or both, calcic deposits and all diseases which affect the 
circulation such as drugs and auto intoxication, and as among 
the local causes catarrh, fistulae, salivary calculus, irritation 
from foreign substances, which are included as modern dentis- 
try, such as detached bristles from the tooth brush, too great 
friction in brushing, injudicious use of the toothpick, the use of 
ligatures and regulating apparatus, application of the rubber 
dam and clamps, artificial dentures and regulating plates, ac- 
cumulation and decomposition of food under artificial dentures, 
and at the necks of the teeth, drugs which over-stimulate the 
parts, the use of tobacco, fillings extending beyond the cervical 
margins, digestive derangements, contagion from unclean in- 
struments, and improper mouth washes and tooth powders, 
especially charcoal. In a word, whatever irritates the gums, 
alveolar process and peridental membrane is likely to produce 
the lesion under consideration. The devitalization of pulps and 
the filling of roots, which throw increased work upon the mem- 

M American System of Dentistry. 
23 Dental Cosn'ios, Vol. XXVIII. 



brane, are also to be accounted as among the factors responsible 
for this pathological condition. 

Talbot pointed out that the disease is contagious so far 
as one tooth becomes infected from another in the same mouth. " 

Of the status of this disease at the close of the year 1887, 
the following analytic picture was drawn by W. X. Sudduth 2i : 
"Pyorrhoea alveolaris is a term applied to the secondary stages 
of a disease that has its inception in a catarrhal stomatitis. Be- 
ing confined, as a rule, to the margin of the gums surrounding 
the teeth, it might be called a 'gingivitis,' were it not for the 
general catarrhal tendency shown by the entire mucous mem- 
brane of the mouth and nasal passages. The intimate relation 
between a general catarrhal idiosyncrasy and pyorrhoea alveo- 
laris is more than mere coincidence. ' ' Its common occurrence in 
persons who have irregular teeth has also been often noted by 
Dr. Sudduth, who considers that this fact has, besides the matter 
of uncleanliness, a direct bearing upon its pathogeny. It is well 
known that the irregularities of the teeth present an indication 
of a degenerative taint, and that persons in whom irregularities 
occur are very prone to catarrhal affections of the respiratory 
organs, including the nasal passage. Their skin is usually very 
susceptible to inflammatory affections. Another feature is the 
offensive ordor of the saliva of individuals who show this partic- 
ular tendency to catarrhal affections even in persons who take 
most scrupulous care of the teeth. In the majority of cases, 
pyorrhoea is a stomatitis in which the local and constitutional 
factors in the production of the disease are largely dependent 
upon hereditary catarrhal dyscrasia for their ability to engraft 
themselves upon the tissues. This position is borne out by the 
clinical experience of Patterson, of Kansas City, Missouri, who 
reports thirty-eight cases of well marked pyorrhoea observed 
by him, thirty-three of which presented undoubted evidence of 
nasal catarrhal conditions; two were the result of direct irri- 
tation of misfitting partial plates, and the remaining three were 
apparently caused by calcific deposits. Patterson remarks that 
a close examination of the history of the above quoted cases 

M Sajous' Annual, 1888, Vol. Ill, page 365. 

confirms the opinion that the disease is, as a rule, an "oral 
catarrh. ' ' 

From the foregoing W. X. Sudduth feels justified in class- 
ing the disease as a localized catarrhal stomatitis which may be 
either acute or chronic. Acute catarrhal inflammation of the 
gums begins in circumscribed points which present a bright or 
rose-red color, and which are generally located on the margin 
or the rugae of the palate. There is but little swelling because 
of the dense nature of the sub-epithelial connective tissues. 
The gums present the same stages as are found in inflamma- 
tion of other mucous surfaces — first dryness, followed by an 
increased secretion of mucus. The parts are very sensitive to 
pressure ; the patient complains of an annoying, burning sen- 
sation. The appearance of the gums is noticeably smooth and 
glistening. They bleed easily when the brush is used or even 
during a meal. This stage does not last very long, but soon 
heals by resolution or passes into a chronic catarrhal stomatitis 
in which condition the gums become markedly swollen and tur- 
gid. They present a condition of tumefaction that sometimes 
rapidly passes into hypertrophy; at other times there is an 
indurated appearance that may last for some time. Granula- 
tion tissue may be produced as the result of overstimulation. 
The gums become detached from the necks of the teeth; and 
pockets are formed from which a fetid discharge may be 
pressed, giving a peculiarly disagreeable odor. Bullae are apt 
to form, which, by rupturing in the process of mastication, 
give rise to intense smarting. The tongue constantly seeks the 
surface if the bullae are on the inner side. 

The pathologic changes which take place are, according to 
Newland Pedley, of England, "hypertrophy of the muco-peri- 
osteal fold around the teeth, accompanied by dilatation of capil- 
lary loops, enlargement of the papilla? and rapid proliferation of 
epithelial cells. Later the gums become firm and contracted and 
display increase of fibrous tissue. The changes which go on in 
the socket have not been as yet satisfactorily worked out. The 
examination of the jaws of carnivora, apparently affected with 
pyorrhoea alveolaris, leads to the supposition that osteitis of the 
alveolar process spreading toward the apex of the socket is pres- 


ent. Later the alveolar walls become absorbed and are at times 
more or less denuded, while the fangs of the teeth become coated 
with a layer of thin, hard, green-brown tartar. Ultimately the 
disease progressing, the teeth, one after another, drop out. ' ' 

From what has been said it will be seen that the pathology 
of pyorrhoea alveolaris may be explained in several ways. The 
general causes are local or symptomatic, or both combined. The 
most common cause of catarrhal gingivitis is found in local 
irritation, combined with some hereditary disposition to catar- 
rhal affections. The next greatest etiologic factor is sympto- 
matic — the local manifestation of a constitutional vice. The 
most common manifestation is that of syphilis and of its anti- 
dotes, mercury and potassium iodide, both of which sometimes 
find expression in a localized inflammation which may be the 
starting point for pyorrhoea alveolaris. As a complication of 
the disease in its secondary stages there can be no doubt of the 
action of micro-organisms, but Sudduth does not feel justified 
in conceding to them a position of specificity. 

His position above quoted is sustained by Pedley, who finds 
that in most instances it is due to some constitutional condition. 
The fact that it is often symmetrical and frequently hereditary 
gives support as to this view. It occurs in mouths of patients 
whose health has been undermined by debilitating influences and 
injudicious habits of living. It is a common sequel of malarial 
fever. Young persons recovering from eruptive fevers are some- 
times subjects of pyorrhoea alveolaris. Frequent pregnancies 
are a fruitful source of the disorder. Attention has been lately 
drawn to the shedding of the teeth in tabes dorsalis, but it does 
not, however, seem to be a constant symptom. Pedley 's view, 
although tending entirely toward the constitutional character of 
the disease, does not militate against its catarrhal nature. 

Bland Sutton has found shedding of teeth frequent in rheu- 
matoid arthritis in animals. He has also met with it in mollifies 
ossium and other wasting diseases. Magitot (who views the 
alveolar dental periosteum as a ligament and not of the same 
nature as osseous periosteum) calls the disease symptomatic 
alveolar-arthritis, and mentions especially as causes, chronic 

Bright's disease and glycosuria, in which latter condition the 
phenomenon is absolutely constant. 

Patterson holds that "mouth-breathing has, in his expe- 
rience, been a very common accompanying condition which he 
cannot help connecting with the production of the disease. By 
it the gums are kept dry, their functions destroyed and the way 
paved for catarrhal inflammation. The majority of the patients 
he has been called upon to treat have been otherwise healthy, 
robust persons. From this fact he does not favor the idea of the 
disease being dependent upon constitutional derangement. It 
is, however, a well-known fact that these are the very class of 
people who when irritation is once set up in their system, present 
the most aggravated cases, by reason of their superfluous vital- 
ity. He says he has occasionally met with cases where the local 
condition was evidently aggravated by constitutional derange- 
ment and cure was thereby retarded. The great majority of 
cases, however, have shown no indication of constitutional pre- 
disposition, but have pointed unerringly to local irritation by 
means of which the function of the mucous membrane had been 
destroyed. ' ' 

Syphilis and other affections may engraft themselves upon 
the gums without a predisposition of the parts toward an inflam- 
matory condition, and having disturbed the normal status of the 
gingival margins they pave the way for subsequent disease in 
the alveolus. Certain drugs, such as mercury, phosphorus, lead, 
etc., have a known deleterious action upon the ligamentous at- 
tachment of the teeth. 

In 1890 Miller ~ : ' expressed the opinion that the disorder was 
of a parasitic nature. 

In 1892 C. N. Pierce 26 charged the disorder chiefly to sys- 
temic predisposition and enthusiastically advocated the theory 
of Reese as to the influence of the uric acid diathesis. 

In 1891 W. X. Sudduth " 7 strongly urged the influence of 
lactic acid as a local factor in the disorder. 

M. L. Rhein 2S presented a method of classifying pyorrhoea 

Micro-Organisms of the Human Mouth. 
International Dental Association, August, 1894. 
Ibid., Vol. XIV. 
'The American Dental Association, August, 1804. 



alveolaris in the following manner: "This classification is 
made by prefixing to pyorrhoea an adjective stating the name of 
the disease which is causing the pathological symptoms in the 
oral cavity as 'gouty pyorrhcea,' 'diabetic pyorrhoea,' etc." 

The author, 29 after further researches, makes the positive < 
statement that the etiology of the disease is due to both consti- 
tutional and local causes. He again reiterates and makes the 
positive statement that modern dentistry is producing more 
"pyorrhcea" (interstitial gingivitis) than any other one cause, i 

He again lays stress on the anatomy and physiology of the 
parts involved and that the alveolar process is a transient bony 
structure, simply for the purpose of holding the teeth in place 
after they have erupted; that the gums are rarely found in a 
healthy condition; that the peridental membrane is never in- 
vaded by pus germs so long as it is in a perfectly normal state ; 
that in phthisical patients and those with low vitality and pa- 
tients who have been ill for any length of time, a low form of 
inflammation of the gums extending to the peridental membrane 
and alveolar process with pus infection takes place; that the 
granular debris or calcic deposits in all cases are secondary con- 
siderations in the breaking down of tissue. 

Neurotics and degenerates, whether wealthy persons or those 
confined in institutions, are mostly afflicted. Children as well as 
grown people suffer with the disease. 

In 1897 the author laid particular stress on the poisons cir- 
culating in the blood causing interstitial gingivitis from auto- 

In 1899 he 30 he spoke of the possibility of calcic deposits on 
the roots of the teeth being "calcareous matter absorbed from 
the alveolar process in the immediate vicinity of the root," etc. 
This theory was later confirmed by researches on the alveolar 
process and mentioned in a paper on "Interstitial Gingivitis," 
published in The Dental Summary, 1903. 

John Fitzgerald, 31 in 1899, claimed that "The production of 
pyorrhcea depends upon two factors, a predisposing cause and 

20 The International Dental Journal, April, 1896. 

30 Interstitial Gingivitis or So-called Pyorrhoea Alveolaris, page 169. 

31 Clinical Journal, March 1, 1899. 


a local irritation. The predisposing cause may be tuberculosis, 
syphilis, scurvy, the exhaustion of acute infectious diseases or 
any other source of malnutrition. The exciting cause may be, 
and most usually is, a gingivitis produced in one of the ways to 
be presently described. There is also a pyorrhoea of gouty 
origin, in which the local necrosis of the peridental membrane is 
caused by gouty disease of one of the blood vessels in its sub- 
stance. ' ' 

The views on etiology of this condition have varied, it will 
be observed, from purely constitutional causes to purely local 
causes, inclusive of microbic affections. In the main it will 
be obvious, however, that both constitutional causes, whether 
inherited or acquired, have been regarded as of influence by the 
majority of those who have written on the subject. There has, 
however, been very little exact study of either the predisposing 
or the exciting causes of the condition. Even the impetus given 
the study of etiology by bacteriology and embryology has as yet 
failed to make itself felt to any considerable degree in this 
department of dental pathology. 

In 1903 the author spoke of the alveolar process as being an 
end organ ; he also laid stress upon inflammation of the alveolar 
process as one of the first diagnostic symptoms in constitutional 
diseases in the same year. 

In 1904 he spoke of the pulp as being one of the most per- 
fect end organs in the body. 

In an article, ''Endarteritis Obliterans and Arterial Hyper- 
trophy in the Alveolar Process," 32 the author first called atten- 
tion to the calcic deposits (not tartar) on the roots of the teeth 
and stated that it was "the detritus from the alveolar process." 
In this article, he lays emphasis on the fact that the alveolar 
process is not only a transitory structure but is also an end 
organ which makes it very susceptible to disease. The nerves 
and blood vessels approach a blank wall. The roots of the teeth, 
so far as disease is concerned, are foreign bodies. 

Examination of the alveolar process of animals or human 
suffering from disease, in which the eliminating organs do not 

The Dental Digest, October, 1903. 


throw off the effete matter (autointoxication), especially in 
syphilitic, tuberculous and scorbutic persons, easily reveals this 
morbid state. 

In "Pathology of Eoot Absorption and Alveolar Abscess" 33 
absorption of the alveolar process is always resultant upon irri- 
tation and inflammation. The strong point is emphasized that 
the alveolar process is doubly transitory and also an end organ. 
He also lays stress on the fact that in the constructive stage of 
the alveolar process, at the third and fourth periods of stress, 
the bone will reproduce itself but after the person has obtained 
his growth, very little or no restoration can take place. He also 
states that neuroses or degeneracy in the child has much to do 
with the success of treatment and that autointoxication also 
plays a great part in final results. 

In a paper on "Peridental Abscess," 34 in some of the lower 
vertebrates, there is a continuous succession of teeth called 
polyphyodontia. "When one tooth has performed its function 
it disappears to give way to another. This continues through- 
out life. In all vertebrates, including man, where only two sets 
of teeth are developed, it is called dyphodontia. The alveolar 
process and teeth of these vertebrates, including man, have re- 
tained phylogenetic remnants of the physiologic processes of 
removing transitory structures. Should man live long enough, 
he would normally lose his second set of teeth by osteomalacia 
or juvenile or senile absorption depending on the age of the 
patient. This is a great factor in the transitory nature of the 
alveolar process. 

The author first mentioned autointoxication in an article, 
"Autointoxication in Its Medical and Surgical Relations to the 
Jaws and Teeth." 35 

33 The Dental Digest, 1904. 

M The Dental Digest, June, 1903. 

36 Journal of the American Medical Association, 1897. 



The attempt has been made in the present work to reduce to 
order the chaotic notions as to etiology, pathology and treatment 
which, during the present century, have gathered around the 
morbid condition erroneously entitled Pyorrhoea Alveolaris. 
While even erroneous titles may have their meaning so fixed by 
usage that any danger from the error involved in the title may 
be practically nil, still this is not the case with the title just 
cited. It suggests erroneous etiology, since pyorrhoea implies 
that there must always be a flow of pus, and hence that the dis- 
ease must always result, from infection with pus microbes. It 
implies erroneous pathology and erroneous treatment for the 
same reason. This being the case, such a title is so dangerously 
misleading as to compel in the present stage of dental science its 
modified use as a term for a disease. With a view of clearing up 
this question at the outset by the use of a proper title, I have 
adopted as a designation for the condition hitherto known as 
pyorrhoea alveolaris, the term "Interstitial Gingivitis." To this 
designation (as to all other attempts to express within a small 
space an extended pathology, etiology, prognosis, and clinical 
aspects) there are some objections. The term interstitial is 
used by some pathologists in a limited obscure sense. By the 
mass of dental pathologists, surgeons, physicians, and by med- 
ical lexicographers, the term is employed in precisely the sense 
in which it is used in the present work. The English surgeon 
and lexicographer Quain defines interstitial as follows : "Inter- 
stitial (inter, between; and sto, I stand) ; relating to the inter- 
stices of an organ. The term is applied in physiology to the 
tissue which exists between the proper elements of any 
structure, namely, some form of connective tissue. In 
pathology the word is used in connection with absorption 
when a part is gradually removed without any obvious 
breaking off, and also to indicate the implication of the intersti- 
tial tissues in morbid processes or their infiltration with morbid 
products, as interstitial pneumonia, interstitial hepatitis." 


The Encyclopaedic Medical Dictionary of the American 
Foster, states that interstitial has three significations : First, it 
is applied to a condition disseminated through the substance of 
an organ or part, and to an inflammation affecting the connec- 
tive tissue of an organ ; second, it is also applied to that form of 
growth which consists in the interposition of new elements be- 
tween old ones, instead of in addition to the surfaces ; third, it 
is applied to pathologic processes occupying the space between 
the essential parts of an organ which constitute its proper tissue, 
and is then employed in a sense opposed to that of parenchy- 

A glance at the illustrations demonstrates the validity of the 
application of the term interstitial (in the sense of Quain, Fos- 
ter, and the other lexicographers) to the condition erroneously 
called pyorrhoea alveolaris. 

I have adopted the term gingivitis for reasons which will be 
obvious at the first glance. The philologic objection may be 
made that in it Greek and Latin are yoked together. Practically 
this is no objection, since German, French, as well as English, 
medical authorities employ such terms of mixed origin. Indeed 
the French (Mailhol * for example) apply the term gingivitis to 
the very condition to which I have applied it. In addition, they 
add to it the specific term "expulsive," to designate "a form of 
recession of the gums, accompanied by alveolar osteoperiostitis, 
and the gradual expulsion of the tooth from its socket. " Fos- 
ter 2 suggests the substitution of the term ulitis as more philo- 
logically correct. The term gingivitis, however, has crept into 
such wide use, that it would be futile to attempt to displace it 
for merely philologic reasons. 

The term "gingivitis," however, conveys the idea that the 
disease always begins at the margin and is confined to the gums 
themselves. Here again we have an erroneous conception of 
the pathology of the disease. Thus in the formation of an 
alveolar or peridental abscess, there is an inflammation pre- 
ceding the pyorrhoeic stage. This is an interstitial inflamma- 
tion and the gum tissue is not involved. Again, in inflamma- 

1 Odontalgie. 
3 Foster, op. cit. 


tion due to mercury, lead, copper, brass, drug-, autointoxications 
and other poisonings and irritations, there is an interstitial in- 
flammation of the alveolar process and again the gums are not 
involved until the disease proceeds to a later stage. 

My researches have shown that inflammation may take place 
from irritants or poisons circulating in the blood at any locality 
between the gum margin and the apical end of the root of the 
tooth. This inflammation may terminate in healthy resolution or 
it may go on to abscess with a discharge through a small fistula 
upon the gum which afterwards may heal without pain to the 
patient and the gingival margin may not be involved. 

I have shown microscopic slides with these pathologic condi- 
tions in almost every constitutional disease. An inflammation 
may take place at the end of the root due to irritation or death 
of the pulp. The gingival border is again not involved. Irrita- 
tion with inflammation around the roots of teeth occur in gout, 
rheumatism, syphilis and many other constitutional diseases 
and the gum margin does not become diseased or the seat of the 
inflammation may be at any point on the root and extend to the 
gingival border. 

In all these illustrations the parts are restored to health 
without pyorrhoea alveolaris or even in many cases gingivitis. 
It is in such pathologic conditions that the word "interstitial" 
is added to "gingivitis." By this term, then, we know just 
what is meant. In no other term now in use can we locate the 
inflammatory area. 

The two terms I have employed convey a fairly correct idea 
of the pathologic process involved in both deep-seated and super- 
ficial inflammation, and do not imply erroneous views as to 
etiology, pathology, prognosis and treatment. 

The pathologic conception adopted in the present work audit 
interstitial gingivitis is that the disorder is a local inflammatory 
condition of the gums, or alveolar process, or both, tending to 
accelerate their normal tendency to disappearance at certain 
periods of stress, or involution, of which involution the changes 
produced by old age are a type. In this early senility of the 
gums and alveolar process, for such it may be termed, two 
great types of causes play a part; the exciting and the pre- 


disposing causes. The exciting causes may be purely local, or 
may be local expressions of constitutional states. Thus it will 
be shown that the influence of uric acid when present is exerted 
as a local irritant, and not as a constitutional factor — the theory 
urged so strongly by Pierce. The uric acid hypothesis, once 
very dominant in medicine, is now losing its force. The trend 
of medical opinion is to consider it one of the danger signals of 
autointoxication which assumes prominence because of its ten- 
dency to excite local irritation. It is but one of a number of 
local expressions of constitutional defect. This view of the in- 
fluence of uric acid in etiology the present work will try to dem- 
onstrate. Prominent among etiologic factors which have to be 
reckoned with, are pathogenic germs. In the present work it will 
be shown by all laws of bacteriology (under which investiga- 
tions must be conducted) that there is no specific germ -which 
is capable of producing the disease itself, and furthermore, that 
the pyorrhoea stage of the disease is merely a complication due 
to pyogenic germ infection of the already diseased gums. The 
views of Galippe as to a specific organism will be shown to have 
failed of support by numerous control experiments described in 
the present work. As these have been conducted by different 
experimenters they are free from the personal elements of error 
which vitiate the researches of Galippe, who violated that canon 
of the laws of Koch which compels production of the disease by 
the alleged specific germ. One predisposing factor will be 
shown in the present work to be the nature of the structures 
affected. This in pathology is called local predisposition. The 
gums, alveolar process, etc., will be shown to be transitory 
structures, as well as end organs, in themselves predestined (as 
already stated) to certain changes at certain ages. By the in- 
fluence of the disease, about to be discussed, these changes 
occur prematurely. The influence of the toxic agents (mercury, 
potassium iodide, etc.) will be shown to have been exerted con- 
stitutionally through the central nervous system, their local ef- 
fects being a secondary consequence of this. The same will be 
shown to be the case with conditions like scurvy and autointoxi- 
cation (where the constitutional factor is most prominent), and 
with the great neuroses (paretic dementia, locomotor ataxia, 


etc.). Here, as in the toxic conditions, one great element consid- 
ered is the influence of the constitutional conditions upon the 
nerves governing local blood supply and tissue waste and repair. 
These influences are significantly illustrated in the various proc- 
esses described later which tear down and build up. 

The influence of morbid heredity as a direct factor will be 
shown not to be great. The influence, however, of degeneracy 
expressing itself along the lines of least resistance will appear 
as an ominously important factor. Heredity here, as elsewhere, 
is a warning rather than a destiny. 

The influence of the nervous system on the processes of 
growth and repair, which is called its trophic function, has been 
shown to play a part in both the etiology of the disease and in 
its progress. This function has received but little attention from 
dentists, albeit its influence has been recognized in dental path- 
ology in connection with great neuroses like paretic dementia 
and locomotor ataxia, in which gum disorders occur, followed by 
loosening of the teeth. The pathology of the disease has been 
discussed in the light of established facts of general pathology 
which have been accepted by the leading dental investigators, 
and not merely from a hypothetic standpoint. The disease has 
been regarded as a local exaggeration of certain physiologic 
processes, accompanied by diminution of the intensity of others. 
In the study of this phase of the question, the latest researches 
of dental pathologists as well as original observation and ex- 
periment have been employed. 

Among the many questions which the present treatise is 
believed to settle (so far as experimentation can) is the follow- 
ing : T he question of the influence and nature of its etiology./ 
It is shown that here, as elsewhere in biology, the etiology of 
morbid conditions has many phases ; that in it exciting and pre- 
disposing causes have alike to be considered ; that while causes 
may be constitutional in origin they very often exert their 
action locally; that the disease is not a product of jgivilization - 
nor a product of any one etiologic factor ; that there is no ground , 
yet adduced for believing the disease to be specifically infectious ! . 
and due to a germ of a specific nature ; that in it the germ infec- / 
tion occurs as a consequence of existing disease, and is not the 



cause of the morbid condition, but one of its stages : Pyorrhoea. 
The experiments made, as well as the pathologic and clinical 
data, have been obtained from many observers, so that as many 
control observations should be had as were necessary to elim- 
inate personal elements of error inevitable upon original obser- 
vation and research. In the pathology no statement is made 
which is not demonstrated by corroboratory data, including a 
photograph of the condition. The treatment has been based upon 
the pathology and etiology. Its central idea is that the human 
being must be regarded as something more than his mouth and 
teeth; hence the duty of the dental scientist is, like that of all 
medical scientists, best shown in a prophylactic direction. 



Because of man's advance in evolution and because of the 
local degeneracies thereon resultant, through the law of economy 
of growth whereby one structure is sacrificed for the benefit of 
the organism as a whole, the face, jaws, teeth, gums, alveolar 
process and peridental membrane, being variable structures, are 
predisposed to disease in their very order of evolution. 

The jaws are growing smaller because large ones are not 
required. The structures are changing their shapes to adapt 
themselves to the new environment. Thus — instead of broad 
large jaws with low vaults ; short, broad alveolar processes with 
plenty of blood supply and vitality to resist mastication; teeth 
short, with large bell crowns to give plenty of room between the 
roots for considerable thickness of the alveolar process for the 
nourishment of the peridental membrane and support and pro- 
tection of the gum tissue — small narrow jaws occur with appar- 
ently high vaults; long, slender and thin alveolar processes, 
which are not used in mastication with sufficient force to carry 
the blood for the nourishment of the tissues. The teeth are 
changing their shape, causing the roots to come closer together, 
and thus lessening the area of the alveolar process. 

That the jaws of man are growing smaller is easily demon- 
strated. Scientists claim two types of heads as a starting point 
in the study of head and face deviations, the brachycephalic 
(round) head of the Teutonic race and the dolichocephalic 
(long, narrow) head of the negro. These two primitive types 
of heads possess two distinct types of jaws. The brachycephalic 
head has a large round dental arch; the jaws and dental arches 
may or may not protrude, while the dolichocephalic head has 
large, long, protruding jaws and dental arches. The normal nat- 
ural tendency in the evolution of man is to eventually (owing to 



admixture of races and environment) harmonize these two types 
and produce a mesaticephalic (medium) head, face and jaws. 
The frontal development of the brain in phylogeny is gradually 
causing the skull bones to project forward. Owing to disuse in 
ontogeny the jaws are growing smaller and receding. 

While these changes are gradually going on normally, cer- 
tain factors are brought to bear upon the mother and child which 
increase or diminish the nutrition of the child and bring about 
arrest or excessive development of the face, jaws and teeth. 
These factors are an unstable nervous system x either in parent 
or child or both. 

Fig. 1. — Illustrates the Primitive Head with a Receding Forehead and Protrud- 
ing Face and Jaw. The Second Illustration Shows an Advance in Evolu- 
tion with the Head, Face and Jaws on a Perpendicular Line, While the 
Third Shows a Recession of the Face and Jaws. 

That these views can be verified are easy of demonstration. 
Drop a perpendicular line (Fig. 1) from the supraorbital ridge 
below the lower jaw. It will be found that in most of the prim- 
itive races the jaws will protrude outside the line and the fore- 
head will remain inside the line. As a human face has advanced 
in its phylogeny, the reverse has taken place. 

Thus an examination of ten thousand people in the streets of 
London revealed the fact that in only four and thirteen one-hun- 
dredths per cent of people examined did the jaws extend outside 
the perpendicular line ; twelve and eighty-seven one-hundredths 
per cent on the line, and eighty-three per cent inside the line. 
In an examination of three thousand English school children 
(about ten years of age) ninety-three per cent possessed jaws 

Talbot: Developmental Pathology: A Study in Degenerative Evolution. 


inside the perpendicular line; six per cent on the line and one 
per cent outside the line. An examination of eight thousand 
people of Boston showed six per cent of jaws extending beyond 
the perpendicular line ; fourteen per cent on the line and eighty 
per cent inside the line. The examination of the people of Bos- 
ton was made because they more nearly represent those of Eng- 
land in this country in nationality, environment and influence 
of marriage and disease. It has required more than one thou- 
sand years to bring about these results. A more vivid illustra- 
tion of this change and one that can be easily understood by 
the reader is that which has taken place in the negro in the more 
settled parts of America in two hundred and fifty years. 

An examination of the lowest negro type in Mississippi was 
made for me by Dr. William Ernest Walker of New Orleans. 
His examinations of three hundred and fifty-seven showed the 
facial angle protruded beyond the perpendicular line in ninety- 
seven and five-tenths per cent of jaws, while two and five-tenths 
per cent of jaws examined were on the line. An examination by 
Dr. Arthur R. Dray of six hundred and eighty-six negroes in 
Philadelphia, eighty-three and fifty-seven one-hundredths were 
found outside the perpendicular line, fifteen and ninety-five one- 
hundredths on the line and forty-two one-hundredths inside the 
line. An examination of one thousand and eighty-five in Chi- 
cago, fifty-one and six one-hundredths per cent protruded ; thir- 
ty-one and eight-tenths were on the line and sixteen and six- 
tenths per cent were inside the line. An examination of one 
thousand negroes in Boston by Dr. Eugene F. O'Neill showed 
forty-five and four-tenths per cent outside the line; thirty -nine 
and five-tenths per cent on the line and fifteen and one-tenth per 
cent inside the line. It will be seen, therefore, that in Northern 
and in old negro families, from race admixture and environment, 
there is less protrusion and more recession than in the Southern 
pure negroes. Arrest of the bones of the face is as common in 
old negro families in the North as among the Caucasic races. 

To further substantiate this claim a comparison of the meas- 
urement from the outside of the first molars of the upper jaws 
of modern races with ancient skulls and ancient races may be 
here given. Examinations made by the late Dr. Mummery, in 



1860, of ancient British skulls measured 2.12 inches, maximum 
2.62 inches, with an average of 2.37 inches. The modern Eng- 
lish jaws measure minimum 1.88 inches, maximum 2.44 inches 
with an average of 2.19 inches. The jaws of people living in 
America measure minimum 1.75 inches, maximum 2.52 inches 
with an average of 2.14 inches. The difference between the an- 
cient Roman soldiers and modern Eomans is the same as that of 
the English. 2 The lateral measurements of the pure negro as 
found in Mississippi are minimum 2.25 inches, maximum 2.75 
inches, with an average of 2.51 inches. The lateral diameter of 
modern negroes varies considerably owing to neurasthenia in 
the parents and disease in the child. Some jaws measure as low 
as 1.75 inches. The jaws of modern negroes residing in Boston 
for many generations are not unlike those of the native whites. 

A further demonstration that the jaws are becoming smaller 
is shown by the disappearance of the third molar, or the irreg- 
ularis resultant on its eruption because of want of room, or 
its eruption with pain for like reason. In the primitive races 
it is large and well developed. 

Dr. Charles Ward says a "point in which the jaws of aborig- 
inal tribes, are, as a rule, superior to those of civilized races is 
in the proportion of the horizontal ramus. As pointed out by 
Harrison Allen, the alveolar and inferior border of the jaw tend 
to parallelism in savages, while in civilized races the symphysial 
height is usually greater than the height in the vicinity of the 
molars. This may be due to gradual degeneration of the 
platysma myoides muscle. Of the significance of the 'ante- 
gonium' or 'pregonium' of the same author I am uncertain, 
but incline to the belief that it is a 'stigma of degeneration.' 
Finally, an as yet incompleted study of the relative proportion 
of jaw to skull has convinced me that the jaws of savages are not 
only proportionately but actually heavier than our own, and 
that the 'cranio-mandibular index,' as I term it, which is the 
ratio between the weight of jaw and weight of cranium, rises 
steadily as we descend from semi-civilized to barbarous and 
savage tribes." 

"Thus, while the white males examined gave an index (pro- 

Talbot: Irregularities of the Teeth. 


portion of jaw to skull) of 11.8, the male Australians presented 
an index of 15.4. 

"Absolute size of the lower jaw is greater in savages: Of 
nine aborigines, including seven North American Indians, one 
African and one American negro, six Malays and five Austral- 
ians, all with beautifully perfect teeth, the mean weight of the 
jaw was 102.4 grams. Of eighteen white males the mean weight 
of the jaw was only 83.4 grams. Yet the weight of the skull was 
nearly alike in both classes, being 690.9 grams for the aborigines 
as against 680.5 for the whites. The weight of the lower jaw 
compared with that of the cranium, or the cranio-mandibular 
Index is 15.6 for aboriginal men as against 12.16 for white men. 
It is 46.2 for the anthropoid apes, our nearest living relatives 
among mammals." 

The change in the two extremes of heads, the brachycephalic 
and the dolichocephalic to the mesaticephalic also produces 
change in the shape of jaws in like manner. Instead of the large 
round jaw of the brachycephalic and the long narrow jaw of the 
dolichocephalic, a medium size jaw development also follows. 



The alveolar processes are situated upon the superior bor- 
der of the inferior maxilla and upon the inferior border of the 
superior maxilla. These bones, considered a part of the maxil- 
lary bones often so described by anatomists, should, however, be 
considered from a more careful study of their physiology and 
pathology as practically distinct bones — their structure, func- 
tions and embryology differ so completely from the structure 
and functions of the maxillary bones. The superior and infe- 
rior maxillae are (unlike the alveolar processes) composed of 
hard, compact bone structure. The large, powerful muscles 
attached to them indicate that powerful work is to be accom- 
plished. When fully developed they retain their full size 
through life. The alveolar processes are composed of soft, 
spongy bone of a cancelloid structure. As early as the eleventh 
week of intrauterine life, calcification of the deciduous teeth 
commences, and by the twentieth week calcific material is 
abundantly deposited. Ossification is also rapidly progress- 
ing about the dental follicles. At birth, the sacs are nearly or 
quite inclosed in their soft, bony crypts, and the crowns of the 
teeth upon their outer surface are composed of enamel, which 
is dense and hard. The embryologic phases of the dental shelf 
elsewhere cited 2 indicate this development. 

The alveolar process, being soft and spongy, molds itself 
about the sacs containing the crowns of the teeth and about 
their roots after their eruption, regardless of their position in 
the jaw. While the alveolar processes have grown rapidly, they 
have up to this time developed only sufficiently to cover and 

1 Pyorrhoea Alveolaris. Paper No. 2. The International Dental Journal, April, 

5 Talbot : Irregularities of the Teeth, page 93. 


protect the follicles while calcification proceeds. When the 
crowns have become calcified and the roots have begun to take 
in their calcific material, absorption of the borders of the proc- 
esses takes place in the order of the eruption of the teeth. 
When the teeth have erupted, the alveolar processes develop 
downward and upward with the teeth until they attain th< j 
depth of the roots of the teeth, which extend in most instances 
into the maxillary bones in the anterior part of the mouth at 
least, and the upper and lower teeth rest at a point in har- 
mony with the rami. The depth at which they penetrate the 
bone differs in different mouths. This depends upon the 
length of the roots and the alveolar process. This in turn de- 
pends upon the length of the rami. The incisive fossa, the canine 
eminence and the canine fossa give evidence of this externally. 
These sockets are lined with extensions of the process, thus 
making its upper border irregular. The crypts of the perma- 
nent teeth are located at the apices of the roots of the tem- 
porary teeth. The permanent teeth have large crowns which 
touch each other, forming a line to the posterior part of the jaw. 
These teeth, as they erupt, entirely absorb the alveolar process 
which surrounded the temporary teeth, and as the new set 
comes into place a new process is built up around them for 
their support. 

The process of absorption of the alveolar process and the 
building up of new bone around the first and second set of 
teeth is inflammatory. This then is the beginning of intersti- 
tial gingivitis in the life of every individual. Whether this 
primitive inflammation continues through life or not, will de- 
pend upon the general health of the person and his ability to 
keep his gums and alveolar process in a normal, healthy con- 
dition after the temporary teeth have erupted. 

The permanent teeth require a deeper alveolar process to 
support their roots, which are much longer than those of the 
temporary teeth. Hence the difference in the depth of the 
vault of the first and second sets of teeth. 

The alveolar process of each superior maxilla includes the 
tuberosity, and extends as far forward as the median line 
of the bone, where it articulates with the process upon the 


opposite side. It is narrow in front, and gradually enlarges 
until it reaches the tuberosity, where it becomes rounded. 

The process is composed of two plates of bones (Fig. 2), an 
outer and an inner, which are united at intervals by septa of 
cancellous tissue. These form the alveoli for the reception of 
the roots of the teeth. In some cases the buccal and labial sur- 
faces of the roots of healthy teeth extend nearly or quite 
through the outer bony plate and are covered by the peridental 
and mucous membranes only. 

This plate is continuous with the facial and zygomatic sur- 
faces of the maxillary bone. The inner plate is thicker and 
stronger than the outer, and is fortified by the palate bones. 
The external plate is irregular upon the outer surface, promi- 

Fig. 2.— Diagram op the Superior Maxillary Boxe with the Teeth Removed. 

nent over the roots of the teeth, and depressed between the 
roots or interspaces. 

With the change in the size of jaws there is also change in 
the shape of the vault and alveolar processes. When the den- 
tal arches are large, measuring from 2.25 to 2.50 inches, the 
vaults are low and the alveolar processes are short and thick, 
not only giving stability to the teeth, but also plenty of nour- 
ishment. Now that the dental arches are growing smaller, with 
an average of from 1.90 to 2.00 inches, the vaults are higher in 
proportion, the alveolar processes long and thin. This renders 
the teeth and jaws more susceptible to trophic changes and 
hence to disease. The alveolar process in the anterior part of 
the mouth, in which the incisors and cuspids are situated, is 
much thinner than in the posterior parts. 


The sockets for the incisors and cuspids are conical and 
much larger than any of the other single sockets. The alveolar 
process is longer and thinner than at any of the other teeth. 
The sockets for the bicuspids are flattened upon their anterior 
and posterior surfaces, and near the apices they are frequently 
bifurcated. The sockets of the molars are large at the open- 
ings. About the middle of their length, however, they are 
divided into three smaller sockets for the reception of the roots. 
In the case of the third molar the number of sockets ranges 
from one large cavity to three or four of smaller size. When 
disease attacks the tissues, destruction is, therefore, more rapid 
in its progress in the anterior parts of the mouth than in the 
posterior, where the processes are thicker and more nourish- 
ment is required. 

The septa are very thin at the margin and gradually increase 
in width to the middle of the jaw, where they become thicker, 
and are finally lost in the substance of the jaw. Some septa 
are thicker than others, and where two teeth are widely sepa- 
rated, the width of the septa naturally corresponds to the space 
between the teeth. 

What is true in regard to a change in the size of the jaws is 
also true in respect to the shape of the crowns of the teeth. 
While they are not growing smaller in proportion to the size of 
the jaws, they are changing shapes. Once they were quite bell- 
shaped, giving considerable space between the roots for a thick 
alveolar process, thus rendering support to the peridental and 
mucous membranes, now the shape has changed. The proximal 
surfaces are almost straight, lessening the width and thus allow- 
ing only for a thin septum, with barely sufficient surface to sup- 
port the tissues without material blood and nerve supply. 

The sockets are lined with a thin plate of compact, bony 
substance, extending from the outer and inner plates of the 
alveolar process to the apex, where there are small openings 
for the entrance of the nerve and blood vessels for the nour- 
ishment of the teeth. 

The bony plate has upon its inner surface the elastic peri- 
dental membrane, which acts as a cushion for the teeth, while 
it is surrounded by a spongy bone. 



The teeth are held firmly in their alveolar sockets by the 
peridental membrane. Teeth with one conical root, and those 
with two or more perpendicular roots, are retained in position 
by an exact adaptation of the tissues. Teeth having more than 
one root and those bent or irregular, receive support from all 
sides by reason of their irregularity. Fig. 3 (a section of the 
jaw of a cat) illustrates the relative position of the teeth, peri- 
dental membrane and alveolar process to each other. 

After the removal of the permanent teeth the alveolar 
process is entirely absorbed. Fig. 4 shows how the absorption 
takes place. The teeth have all been removed from the supe- 
rior maxilla and the alveolar process has been entirely absorbed. 

Fig. 3. — Ground Section of .Iaw and Teeth of Cat. (Andrews.) 

The molars on the lower jaw having been extracted, absorption 
of the alveolar process has resulted in marked contrast with the 
anterior alveolar process, which remains intact and holds the 
teeth firmly in place. It is, hence, evident from the changes 
which occur, from the first development of the teeth to their 
final extraction, that the alveolar process exists solely to pro- 
tect the teeth in their crypts during development and after 



eruption. After the temporary teeth are in place the alveolar 
process remains unchanged (except by gradual enlargement in 
harmony with the growth of the maxillary bones) until about 
the sixth year, when the second set appears. The crowns of 
the permanent teeth require more space than those of the tem- 

Fig. 4. — Plaster Casts of the Superior and Inferior Jaws in Position. All the 
Teeth Have Been* Removed on the Upper Jaw, and the Molars and Second 
Bicuspids on the Bower Jaw. Absorption of the Jaws Where Teeth Have 
Been Removed Well Advanced. 

porary set; and the alveolar process must necessarily enlarge 
to accommodate them. This enlargement of the alveolar proc- 
ess is caused chiefly by formation of the crowns of the perma- 
nent teeth before eruption, and to a limited extent only by 

Pig. 5.— Thi 

Anterior Alveolar Process Excess: 
the Teeth Upwards. 

'Ely Developed, Carrying 

growth of the maxillary bones. These may cease development 
at any period of the life of the individual, or continue as late 
as the thirty-sixth year. As diameter of the crowns of the per- 
manent teeth form a larger circle than that of the maxillary 


bones, the alveolar process must necessarily increase its diam- 
eter and present large spaces between the roots of the teeth 
for the development of the alveolar process. 

The process is solely for retaining the teeth, and if for any 
reason the dental follicles should not be present, and the tooth 
should not erupt, or if it should be extracted early, the process 
would not be developed at that point. In my collection of mod- 
els are cases of arrested development of the alveolar process, 
caused by the lack of bicuspid and lateral incisor germs, and by 
extraction of deciduous and permanent teeth. 

If one or more teeth were not to antagonize, the alveolar 
process would extend beyond the natural border, carrying the 
teeth with it. A marked illustration of this is seen where the 
molars are decayed to the gum and the roots remain. The 
vascularity of the process may be such that hypertrophy re- 
sults. Excessive development of the alveolar process is fre- 
quently observed by every practitioner in connection with the 
anterior inferior teeth. When the articulation is normal, occlu- 
sion of these teeth never takes place. Frequently (especially 
in patients from six to twelve years of age) these teeth extend 
to and occlude with the mucous membrane of the hard palate. 
Such a case is illustrated in Fig. 5. This model is taken from 
the jaw of a person thirty-seven years of age, but this excessive 
development took place between the ages of six and twelve 
years, since at that period the vascularity of the tissues is more 
vigorous, and the development of the process more formative 
than at any period subsequent to the development of the first 
permanent teeth. 

In one patient under observation the incisors and cuspids, 
together with their alveolar process, are situated upon the 
external surface, while the bicuspids, molars and their alveolar 
process are located upon the inner border of the jaw. In an- 
other patient, the alveolar process failed to cover the roots of 
the bicuspids and molars upon the outer surface, the teeth hav- 
ing forced themselves into a larger circle through the alveolar 
process by the contact of the crowns. The roots in this patient 

8 Dental Surgery, page 44. 


can easily be outlined by the finger through the mucous mem- 
brane, the outer plate of the alveolar process barely, if at all, 
covering them. Tomes 3 illustrates a patient of faulty develop- 
ment of the outer plate of the alveolar process, exposing the 
crown of the temporary teeth. This occurred in a hydro- 
cephalic. I have a number of models showing the anterior alve- 
olar process projecting beyond the normal position through the 
forward movement of the molars. This may be due to a nat- 
ural movement of the molars forward, or the process may be 
forced forward by the improper occlusion of the jaws. The 
teeth are moved from one position to another simply by the 
force consequent upon absorption and deposition of bone. This 
is noticeable in the spaces between the centrals, when the alve- 
olar process develops to a larger circle than is necessary to 
accommodate the teeth. The alveolar processes are influenced 
in one direction or the other by the pressure of articulation. 
This results from inharmonious development of the jaws. The 
teeth may come together in such a manner as to throw the 
alveolar processes either to the right or the left, thus produc- 
ing a full, round arch upon one side of the jaws, and a perfectly 
flat or straight arch upon the other. Occasionally both upper 
and lower alveolar processes are carried forward in the same 
manner. The alveolar process upon the lower jaw is more 
liable to be found upon the inner border of the jaw than is the 
upper alveolar process, as the inferior maxilla is larger and 
more dense than the superior, and when the teeth are once in 
position upon the lower jaw they are not so liable to subse- 
quent change. Owing to this the teeth of the superior maxilla 
do not form so great a circle. This causes the teeth upon the 
sides of the jaw to conflict, and the lower teeth and alveolar 
processes to be carried in, while the anterior teeth of the lower 
jaw are held inside of the superior anterior teeth, thus carry- 
ing the alveolar processes inward. 

The teeth are continually changing their positions in the 
mouth. This is as often beneficial as it is detrimental. That 
the teeth may perform their full function, they should not only 
remain firmly in the alveolar process, but they should also 
antagonize properly. The teeth may be compared to the bricks 


in an arch. Eemove a brick and the arch falls to pieces. It is 
frequently found that the teeth do not articulate properly; by 
a slight movement, or by cutting away the grinding surfaces, a 
better articulation may be secured. When this operation is per- 
formed, the teeth move in their sockets by absorption and depo- 
sition of bone, demonstrating the fact that the process changes 
in shape and substance. Ziegler 4 says absence of functional use 
is a frequent cause of premature lacunar absorption of the 
bone. This form of atrophy from disuse occurs not only when 
a limb or a part of a limb is deprived of its normal activity, 
but also when portions of a single bone cease to perforin their 
function of support, and finally, like all the bones of the body, as 
age advances, normal or physiologic absorption takes place, 
while the teeth are still in the jaws. Unlike other bones of the 

Pig. G. — Hypertrophy op the Entire Alveolar Process. 

body, however, the absorption of the alveolus progresses to a 
greater extent because of the unstable condition of the struc- 

From what has already been said of the vascularity of the 
alveolar process, it is evident that hypertrophy of the tissue may 
ensue from an unbalanced nervous system and from simple irri- 
tation of varying degree. This unbalanced nervous system may 
act directly upon the pituitary body, producing hypophyseal 
disorders which in turn affect the growth of the jaws and alve- 

* A Text-Book of Special Pathological Anatomy, page 145. 



olar process. The irritation consequent upon the eruption of 
the teeth, together with the excessive blood supply, are both 
primal causes of overbuilding of tissue, i. e., hyperplasia. 

The ragged roots of the temporary teeth, produced by ab- 
sorption of the gases from the putrescent pulps, and the pres- 
sure of the permanent crowns against the tissues, produce suf- 
ficient stimulation to excite physiological action. Tissue-build- 
ing generally is seen in connection with all the teeth, and the 
process becomes unnaturally thick, the teeth frequently are 
carried in one direction and another; cementosis of the roots 
of the teeth and hypertrophy of the process result. 

In cases of hypertrophy of the alveolar process, enlarge- 
ment is associated with the inner plate of the alveolar process. 
In patients coming under my observation the inner plate in 

-Hypertrophy of the Alveolar T'ro 
Superior Molar Teetl 

ess Around the Left 

most is the part of the alveolar process affected (Fig. 6 case). 
The outer plate, although quite irregular from the arrange- 
ment of the teeth, is usually normal in thickness. This dis- 
parity in the two plates of the alveolar process is due to the 
fact that the inner plate of the alveolar process possesses a 
large blood supply, the posterior or descending palatine arter- 
ies furnishing the ossific material. I have observed but few 




patients where hypertrophy has extended to and included the 
outer plate. When the outer plate becomes involved the alve- 
olar process assumes a very thick condition. Occasionally 
hypertrophy will affect one side only or one distinct locality 
(Fig. 7). In this patient the enlargement is upon the* left side 
and extends from the first bicuspid posterior to and including 
the maxillary tuberosity. Instead of the force being directed 
inward, as is generally the case, the process is forced outward 
and backward. This enlargement occurred previously to the 
development of the second and third molars. The alveolar 
process extends downward and occludes with the teeth upon 
the lower jaw, thus preventing the molars from erupting. 

The causes which produce hypertrophy of the alveolar proc- 
ess are those due to an unstable nervous system. This subject 
is discussed in my work on "Developmental Pathology: A Study 
in Degenerative Evolution." 

(Late researches have shown that the hypophysis and its 
disorders have much to do with arrest and excessive develop- 
ment of the body as a whole or of particular organs or struc- 
tures of the body. The author many years ago called the atten- 
tion of the profession to the fact that an unstable nervous sys- 
tem of the parent or disease in the child after birth produced 
excessive or arrest of development of the tissues. It is possible 
that the unstable nervous system of the parent or the diseases 
of the child act first upon the pituitary body, which in turn 
acts upon the tissues themselves or that they both act together.) 



Under the microscope, two systems of Haversian canals are 
seen in the alveolar process. Kolliker 1 describes these as fol- 
lows : 

"The Haversian canals are of two kinds. One with the 
regular lamellae system surrounding it, and the other, the so- 
called Volkmann's canals, containing- the perforating vessels 
from Von Ehner, which have no surrounding lamella?, but sim- 

Fig. 8. — Section of Bone Showing Blood Vessels of Von Ebner (Kolliker). 

ply penetrate through the layers of bone. Volkmann's canals 
are present in all tubular bones in old and young. While espe- 
cially present in the outer basal lamella?, they occur also in the 
interstitial leaflets and in the inner chief lamella? as well as in 
the periosteal layers of the skull bone. Here their number is 
very variable (Fig. 8). They run partly transversely or 
obliquely, and also partly longitudinally, through the lamellae. 

Handbuch der Gewehelehre, page 272. 



Many of these canals open in the outer or inner surfaces of the 
substantia (compact substance), and also here and there in the 
Haversian canals, and form altogether usually a wide-meshed 
irregular network. In their structure they are sometimes 
smooth and sometimes furnished with dilatations and angles 
projecting in and out in profile. The widest has a diameter of 
100 micrometers or more, and the narrowest not more than 10 
or 20 micrometers, and there are still narrower ones which are 
altogether obliterated, appearing like rings or circular-formed 


Fig. 9. 

-Section op Bone (Higher Magnification) Showing 
Blood Vessels of Von Ebnek. 

structures without any lumen, or like those far from rare oblit- 
erated true Haversian canals first described by Tomes and 
de Morgan. The contents of the Volkmann canals are the same 
as the Haversian canals." 

Fig. 8 is a cross section of the medulla of a calcified human 
humerus slightly changed. The outer lamellae contains a large 
number of Volkmann 's canals running longitudinally and trans- 
versely and extending through the outer plate of bone into the 
periosteum. Fig. 9, the cross section of the section seen in 

THE ALVEOLA!! I'lMX'ESS l/NDEK THE 1IR IK >S< < >l ' i: . 


Fig. 8, shows these canals more highly magnified. The Haver- 
sian canals are large round spaces (Fig. 10), containing -a sin- 
gle artery and vein. The fine hair-like spaces running from 
these large spaces are the canaliculi. The dark spots circulat- 
ing each Haversian canal are the lacuna?. The canaliculi run 
from one lacunae to another or into a Haversian canal or they 
anastomose with each other. The rings of bone about each 
Haversian canal are called lamellae. The lacuna? seem to be 
about uniformly distributed throughout the bone. The spaces 





■< V V*- // 

\-% tjtj. r e f 

Pig. 10. — Transverse Section of the Diaphysis of the Humerus 

Magnified 350 Times. 

A, Haversian Canal. Dark Spaces, Lacunar. 

Hair-like Spaces. Canaliculi. 

Fig. 11. — Longitudinal Section of Bone Magnified 100 Times. 

between the lacunas and canaliculi are filled with lime salts. 

A longitudinal section of bone (Fig. 11) is similar in appear- 
ance to the cross section. Instead of the lacuna? being arranged 
in rows around the Haversian canals they are parallel. It will 
be noticed that the Haversian canals run in different directions 
and communicate with each other at certain intervals. The 
foregoing description, with illustrations from Kolliker, is essen- 
tially that of the minute anatomy of the alveolar process. 




The tooth, according to Minot, 1 is a papilla which projects 
into the epidermis, and ossifying in a particular way, changes 
into ivory around the soft core or pulp. To the papilla the epi- 
dermis adds a layer of enamel. The tooth proper unites with 
a small plate of dermal bone at its base. By a modification on 
the jaw, the epidermis first grows into the dermis, and then 
the dermal tooth papilla is developed. The teeth were primi- 
tively organs of the skin and widely developed over the sur- 
faces of the body. As the mucous membrane is practically a 
continuation of the skin, it, in accordance with the law of indi- 
viduation, became specialized and lost some of the functions 
of the skin while developing the others to greater perfection. 
The mucous membrane lines the cavity of the mouth, the 
nose, and extends through the larynx into the lungs and through 
the oesophagus into the stomach. It covers the tongue, jaws, 
alveolar process, dipping down between the necks of the teeth 
and the alveolar process as far as the peridental membrane, 
leaving a free space between the membrane and the teeth 
through its entire length. 

It consists of two layers (Fig. 12), the epithelium (A) and 
corium (B), separated by the basement membrane (C). The 
epithelium is composed of the epithelial cells : First, one row of 
columnar cells (D) situated upon the basement membrane (C) ; 
second, two rows of six-sided prickle shells (E) ; third, two rows 
of six-sided cells (F) ; fourth, two or three rows of squamous 
cells (G) ; and fifth, four or five rows of flattened dead cells (H), 
which were originally the columnar cells upon the basement 

Embryology, page 481. 



membrane. The young new cells are the columnar cells which 
pass from one stage to another, changing their shapes until they 
eventually become dead cells and are exfoliated from the surface 
of the tissue. The basement membrane (C) is made up of fibers 
running longitudinally, from papilla 3 , which allow the tunica 
propria containing blood vessels and nerves to pass up into the 
epithelium structure. 

Fjg. 12. — Diagrammatic Illustration of the Epithelium and Submucous Layers 
of the Mucous Membrane. 

A, Epithelium. B, Corium. C, Basement Membrane. D, Columna Cells. E, 
Prickle Cells. F, Six-sided Cells. G, Squamous Cells. H, Flattened Dead Cells. 

The corium (B) (which lies below the basement membrane) 
is composed of alveolar connective tissue, white yellow fibrous 
connective tissue, muscular fibers, nerves, blood vessels and 
lymphatics. It is made up of the tunica propria and the sub- 

The tunica propria (beautifully shown in Fig. 13) consists 


of interlacing' connecting fibers interspersed with much elastic 
fibrous tissue. This tissue penetrates the epithelial layer in the 
form of cone-shaped papillae, varying in length with the thick- 
ness of the epithelium. This layer being the thickest at the 
gum margin (E), these papillae are the longest and largest at 
this locality. The fibers of the tunica propria pass gradually 
into the submucous membrane (G), and from there into the peri- 
osteum and peridental membrane (M), so that it is difficult to 
determine the mucous capacity line of demarcation separating 
the different structures. The submucosa is composed of fibrous 
connective tissue of a much less compact variety. This struc- 
ture is attached to the bones through the periosteum and peri- 
dental membrane. In this structure the glands, blood vessels, 
nerves, fat cells, etc., occur. 

The larger blood vessels (K) are found in this structure. 
From these large blood vessels small capillaries extend to the 
tunica propria. It is here that inflammation commences in 
interstitial gingivitis when due to local irritation. Numerous 
veins accompany each artery, and lymphatics form a network 
around them. Small nerve filaments are also in this structure, 
which pass through the tunica propria and into each papilla in 
connection with the capillaries. The terminal nerve fibers come 
in contact with the muscular fibers, so that there is direct com- 
munication by blood vessel and nerve throughout the mucous 
membrane from the nose, stomach and lungs. The gum tissue 
is very thick and made up of fibrous tissue running in three or 
four directions, rendering it dense, tough and hard. The mem- 
brane thus differs from the same structure in other parts of the 
body. On account of these numerous fibers, this structure is 
bound tightly to the alveolar process. The gum tissue acts as 
a cushion and protection from irritation which may arise from 
hard substances being taken into the mouth. As this membrane 
passes and coalesces with the membrane of the lips and cheeks, 
it becomes much thinner and less dense. In the center of the 
tooth, the parallel fibers in the tunica propria are composed of 
flattened fasciculi of connective tissue. There are three sets 
of fibers — those which run vertically, those which radiate and 
are fan-shaped, and those which are horizontal. 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-tl 

Fig. 13. — Longitudinal Section of Tooth and Gum Tissue. 


D, Dentine. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. M, 
Fibrous Tissue. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue 
and Peridental Membrane. RR. Space Pocket from Want of Union of the Epithelial 


The mucous membrane, like the alveolar process and peri- 
dental membrane, is composed of very unstable tissue. It 
changes its structure, blood vessels and nerve system as often 
as the other structures. Its blood vessels and nerve system are 
continually renewing connective tissue, periosteum and periden- 
tal membrane. 

A difference is noted in the structure of the papillary layer 
in man and the lower animals, such as the dog, the sheep and 
the calf. In man the gum tissue is not so thick, therefore the 
papillae are broader and shorter, while in the lower animals the 
papillae are narrow, long and more closely set together. Blood 
vessels and nerves are not so numerous and close together in 
man as in animals. 


The periosteum is a fibrous tissue covering the outer surface 
of the alveolus. The peridental membrane is composed of simi- 
lar structures covering the roots of the teeth and lining the 
inner wall of the alveolus. They are both derived from the 
mesoblastic layer. For this reason there can be very little dif- 
ference in the character of the structure of each, except so far 
as function is concerned. The periosteum is made up of four 
different kinds of fibers. An outer layer of coarse, white fibrous 
tissue, an inner layer of fine, white fibrous tissue, elastic fibers, 
and penetrating fibers (fibers of Sharpey). 

The fibers of the periosteum are coarser than those of the 
peridental membrane. The coarser fibers run parallel with the 
alveolar process (J) over the border and extend as far as the 
union of the epithelial layer (E) and the periosteum (H), Fig. 
14. ("The dental ligament," Black. 2 ) The finer fibers run in 
all directions and enter the alveolar process at every point. If 
a section of the alveolar process treated with acids or a section 
affected by halisteresis or osteomalacia be placed under the 
microscope, the fibers are seen to retain the original shape of 
the bone. 

a American System of Dentistry, page 

X 75. A. A. olvj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 14. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
brane and Periosteum. Normal Tissue. Sheep. 

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. 
H, Periosteum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, 
Fibrous Tissue. AA, Point of Union of Epithelial Tissue and Peridental Membrane. 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 15. — Cross Section of Tooth, Alveolar Process, Peridental Membrane 
and Periosteum. Normal Tissue. Dog. 

B, Dentine. C, Cementum. D, Pulp. H, Periosteum. J, Alveolar 
K, Capillaries. M, Fibrous Tissue. U, Nerve Tissue. CT, Connective Tissue 


The fibers of the periosteum, therefore, are continued 
throughout the process from the periosteum on the one side to 
the peridental membrane on the other. This is also illustrated 
in the mouths of persons, where (after wearing artificial den- 
tures for a short time) heat produces absorption of the lime 
salts, leaving the fibrous tissues intact. 

The periosteum is abundantly supplied with blood vessels 
which anastomose with each other and enter the alveolar proc- 
ess at the Haversian canals. The plexus of blood vessels is much 
larger proportionately in connection with the alveolar process 
than with other bones of the body, owing to its transitory 

The peridental membrane commences at the margin of the 
epithelium at the neck of the tooth AA, Fig 14, and is attached 
directly to the cementum. This membrane has various func- 
tions: First, it fills the space between these two structures, 
forming a cushion for the teeth to rest upon; second, like the 
alveolar process, it is present only when the teeth are present, 
and therefore develops with the alveolar process when the first 
teeth erupt, it is entirely lost when the temporary teeth are 
shed, is restored with the eruption of the second set, and when 
the permanent teeth are extracted it disappears with the alve- 
olar process completely; third, it furnishes the nourishment for 
the teeth while they are in position in the jaw, and holds them 
in their sockets. 

The fibrous tissue, in its earliest stages comprises nearly all 
or quite all of that portion of the jaw which eventually becomes 
the alveolar process. Calcification begins at the center of the 
jaws and gradually closes in upon the fibrous membrane until 
it becomes the thickness of a sheet of paper. In young persons 
the membrane is much thicker than in old age, since, as age 
advances, the osteoblasts on the one hand and the cementoblasts 
on the other send out new material and each wall closes in upon 
the membrane, which becomes very thin in old age and almost 

The fibers which compose this membrane extend in all direc- 
tions ; some crosswise penetrating the cementum, on the one 
hand, and the alveolar process on the other. In a general way, 


since the fibers extend through the alveolar wall, they are more 
closely adherent to the bone than to the cementum, and usually 
cling to the latter when the tooth is removed. It will be observed 
that these fibers do not enter the alveolar process uniformly as 
claimed by Gray 3 and Pierce 4 , like tacks or nails driven regu- 
larly into a board (the "fibers of Sharpey" Fig. 14), but vary 
as to quantity in different localities. In some localities they 
penetrate in large quantities and almost surround a piece of 
alveolar process, while a few fibers penetrate but a short dis- 
tance. In some places, they can be traced almost through the 
alveolar process. These fibers are much finer in man (Fig. 15) 
than in the lower animals (Fig. 14, dog). In connection with 
the fibers which pass into the alveolar process are numerous 
blood vessels. Others run diagonally, and still others length- 
wise, all making up a tissue which holds the tooth in position in 
the jaw. The fibers enter the peridental membrane at all points 
of the process, from its margin to the apex of the roots. The 
elasticity of this membrane is so great that in correcting irregu- 
larities a tooth may be turned from one-fourth to one-half 
around without breaking the fibers. The elasticity is greatest 
in youth. As age advances, the membrane grows thinner and 
thinner until, late in life, there is almost a bony union between 
the tooth and the alveolar process, thus preventing stretching 
of the fibers. At the upper border, under the gum tissue, these 
fibers extend over the edge of the alveolar border and unite 
with the fibers of the periosteum on the outer border of the 
process, forming the interstitial tissue. 

If absorption of the inorganic substance of the alveolar 
process occurs, the fibrous tissue retains the shape of the proc- 
ess. The same results when inflammation of the peridental 
membrane takes place at the gum margin or at the apex of the 
root of the tooth. What was once alveolar process is now peri- 
dental membrane or fibrous tissue. 

Two kinds of structures are present in the alveolar process 
— a dense, compact, hard structure (composed of lime salts), 

1 Anatomy. 

1 American System of Dentistry, page 668. 

X 75. A. A. obj. 

Micro-photographs, reduced one-third. 

-Cross Section of Tooth, Alveolar Process and Peridental Membrane. 
Injected Blood Vessels. Normal. Dog. 

B, Dentine. C, Cementum. I, Peridental Membrane. 
Capillaries. L, Haversian Canals. 

J, Alveolar Process. K, 

X 7.3. A. A. obj. Zeiss. Mi 

duced one-third. 

Fig. 17. — Cross Section of Tooth, Alveolar Process and Peridental Membrane. 
Injected Blood Vessels. Normal. Dog. 

B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. K, 
Capillaries. L, Haversian Canals. 


and a fibrous tissue; either alone will retain the shape of the 

Blood vessels permeate this membrane throughout from the 
gum tissue at the neck of the tooth, through the alveolar walls 
to the end of the roots. They are most abundant in youth. 
Capillary blood vessels enter the Haversian canals through the 
process and into the cementum. Many of these blood vessels 
extend the entire length from the gum margin to the apex in 
straight lines and vice versa. In many of the illustrations, the 
blood vessels will be seen to follow the line of the alveolar 
process (Fig. 14). A great supply of blood vessels penetrate 
the membrane through the alveolar walls. These vessels unite 
and anastomose with the arteries which traverse lengthwise, 
forming a complicated plexus (Fig. 16). According to some 
writers the vascular supply of the peridental membrane is situ- 
ated in the center of the structure. This has not been my expe- 
rience. All of my slides, as well as those here presented, show 
the blood vessels to be situated nearest the alveolar process. It 
is quite natural that this should be so, since very little blood is 
required for the nourishment of the cementum, while the larg- 
est amount is required to supply the alveolar process. The sys- 
tem of blood vessels situated in the peridental membrane and 
shoving their relation to the surrounding tissue is well shown 
in the injected specimen from healthy dogs (Figs. 16 and 17). 
Pus pockets and abscesses are hence more liable to form near 
and in the alveolar process than near the tooth structure. When 
infection takes place, the products of inflammation are carried 
through the blood vessel and the foci of round cell inflammation 
are located near or in the alveolar process where abscesses form. 
The vessels seen in the membrane anastomose very freely with 
those at the gum margin, showing the membrane to be well 
nourished in all its parts. Should one part become involved by 
disease the other parts are overnourished in consequence. 

These blood vessels enter the alveolar walls with the fibrous 
tissue through the Haversian canals and these in turn permeate 
the entire bone. As age advances, however, the bone becomes 
more dense, and the Haversian canals become smaller and 
(under certain conditions) cease to exist. When disease takes 



place, either at the gingivus or at the apex of the root, the sup- 
ply of blood being thus cut off, the tissues receive sufficient 
nourishment through the alveolar wall. Since the structures are 
in a transitory state, being destroyed and repaired so fre- 
quently, it is evident why the blood supply is so rich. 


Small, hard bodies are frequently found in the peridental 
membrane. These are sometimes in the form of concentric 
rings of lime salts and are called calcospherites. They are not 
always round, but may be of any shape and vary as well in size. 
They bear the same relation to the peridental membrane that 
pulp stones do to the dental pulp. Black 5 says: "I have seen 
more of them about the roots of the molars than elsewhere, 
but have found them along the sides of the roots of the bicus- 
pids." When irritation and inflammation take place in the 
peridental membrane, the cementoblasts build up cement sub- 
stance, just as the osteoblasts do in the alveolar process and 
the odontoblasts do in the pulp chamber. Sometimes they are 
attached to the root of the tooth, producing a condition called 
exostosis or cementosis. They may remain unattached, float- 
ing in the fibrous tissue. These are very common in connec- 
tion with interstitial gingivitis. 


A somewhat widespread opinion locates special glands in 
the gingival tissues and the peridental membrane. This seems, 
to a certain extent, to be in part due to the lack of definite 
knowledge as to the etiology of interstitial gingivitis, and in 
part to the fact that certain constitutional conditions, such as 
mercurial and potassium iodid poisoning and scurvy, manifest 
themselves in the gum tissue in a way similarly to their action 
in the glandular structures of the body. Black 6 claims, for ex- 
ample: "That part of the gingival margin that lies in against 
the neck to the tooth is of a different structure from its other 

Periosteum and Peridental Membrane, page 9- 
American System of Dentistry, pages 955-956. 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 18. — Longitudinal Section of Gum. Normal Tissue. Sheep. 

C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. 
M, Fibrous Tissue. AA, Point of Union of Epithelial Tissue and Peridental Mem- 
brane. Nm, Nasmvth 's Membrane. Sg, So-called Glands of Serres. 


parts. Here it is clothed with a very soft, round or polygonal 
gland-like epithelium that suggests the formation of a gland, 
but fails to assume the glandular structure, though it seems to 
have been regarded as such by Serres. This — which I shall call 
the gingival organ — emits a profusion of small rounded cells 
which are always found in the saliva (Salter) and are usually 
called mucous corpuscles. It is well known that certain glands 
have the power of the selection and excretion of certain poi- 
sons, and in this way of eliminating them from the system, and 
that if the substance be in large amount, hyperemia, or even 
inflammation, may result. It is also known that mercury and 
potassium iodid will produce inflammation of the free margins 
of the gums, and Salter has found these cells are in greater 
abundance under these circumstances ; also that the cells taken 
from the gingival border and submitted to chemical tests after 
the person has taken potassium iodid are found to yield and 
are tinged with iodin." 

Longitudinal sections of the tooth, alveolus and surrounding 
tissues, under the microscope, exhibit a very peculiar formation 
of the mucous membrane at its line of union with the peridental 
membrane at the neck of the tooth. Black 7 (in an article beau- 
tifully illustrated by Frederick Noyes) seems to identify these 
with the so-called glands of Serres or gingival glands (Fig. 18). 
He speaks of them as glands in various places throughout the 
article; for example, "But little can now be said of the func- 
tion of the network of glands of the peridental membrane, be- 
yond what is indicated by their form, location and histological 
characters. With the knowledge of their position and general 
character, clinical observation leads to the conclusion that they 
are readily disturbed by certain drugs, notably by mercury and 
iodin ; and that they are often disturbed by substances poison- 
ous to them floating in the blood streams. This is evidenced 
by the appearance of marginal gingivitis, with soreness of the 
peridental membrane. Such disturbances would not be likely 
to occur without the presence of some specialized or secretory 
tissue. ... It seems to me verv certain that the disease 

Dental Cosmos, February, 1899. 



which I have described as phagedenic pericementitis has its 
seat in these glands." Black, however, does not seem quite"cer- 
tain of the validity of his position, since he further remarks, 
"Though definitely lobulated, this body does not seem to pos- 
sess the characters of a gland, and I should not suppose from 
an examination of its tissues that it had a glandular function. 
It encircles but a portion of the neck of the tooth, usually only 
the approximal portion, thinning away toward the buccal and 
lingual, so that in many of the lengthwise sections it may be 
very small, or does not appear at all." 

In many slides of sections from canine jaws and human, 8 the 
same peculiar arrangement of structure was observed, although 
not in so marked a degree. In the immature herbivora (calf and 
lamb) these peculiar formations of structure are well marked, 
albeit less so in the carnivora, and still less in man. 

Were glands present in this locality it is logical to infer that 
they would become involved in mercurialism, plumbism and 
scurvy, and exhibit marked inflammation with broken-down 
structures in a given locality, as at the union of the gum tissue 
with the peridental membrane. Such a case is unknown. 

The mucous membrane under the microscope appears at a 
point between the teeth (and faintly so at the inner and outer 
border as shown by Black) to double upon itself. When the 
tooth erupts, absorption of the gums occurs at the highest point. 
The gum tissue passing down to the neck of the tooth folds or 
crowds upon itself between the teeth with a peculiar curve 
downward, inward and then outward and upward. At the upper 
border, about midway from the gingival margin to the neck of 
the tooth, may be seen a space or pocket (never twice alike in 
appearance) where the edge of the gum tissue comes in contact 
with the original epithelium. Sometimes the space or pocket is 
closed up (Figs. 48, 49, 57). Again it remains open (Figs. 13, 
37, 56, 59). Frequently this peculiar type of structure is absent, 
showing that the fold of gum tissue either has been absorbed in 

8 The material obtained for making slides from man, other than the scurvy eases, 
was obtained through the kindness of surgeons from jaws removed from hospital 
patients, as a result of disease; the surgeons placing them into alcohol or Miiller's 
solution as soon as removed. 

A. A. 

Micro-photographs, reduced one-third. 

Fjg. 19. Cross Section of Tooth and Peridental Membrane. 
Normal Tissue. Sheep. 
C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 

300. No. 2 projection ocular. D. D. obj. Zeiss. Micro-photographs, 

reduced one-third. 

Fig. 20. — Cross Section of Tooth and Peridental Membrane. 
Normal Tissue. Sheep. 

C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 



the eruption of the tooth or did not form. This peculiar form 
encircles only a portion of the neck of the tooth (according to 
Black's examination of the structure in sheep). This in itself 
seems to offset the glandular theory, since gingivitis almost in- 
variably starts on the lingual or palatine and labial surfaces 


X 560. No. 2 projector ocular. One-twelfth obj. Zeiss. 

Fig. 21. — Cross Section of Tooth and Peridental Membrane. 
Normal Tissue. Sheep. 

C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 

where this structure does not appear. In the slides of the scurvy 
case there does not appear the slightest evidence of anything 
resembling glandular structure. Hence it would seem safe to 
conclude that the glandular structure does not occur in this 


locality. It is by no means impossible that in the peculiar epi- 
thelium in this locality, epithelial cells undergo changes which 
to some observers simulate glandular structure, but on histo- 
logic analysis are distinguishable from it, resembling in this 
the crypts of the head of the penis. 

In cross sections of the peridental membrane, with a low 
power may be seen dark bodies arranged along the margin of 
the cementum in the peridental membrane (Fig. 19). They are 
more numerous, however, near the gingival border than at the 
root extremity. These bodies are more numerous and better 
denned in the sheep than in the calf, and more apparent in the 
canine jaw than in the human. Under higher power (Fig. 20) 
they may be distinctly demarcated as epithelial cells arranged 
in single rows of loops, again in double rows, again in rows of 
three and sometimes in round or oblong groups, with clusters of 
cells without shape or form. With a still higher magnifying 
power (Fig. 21) it will be seen that these masses of cells are 
polygonous, never prismatic. They hence are similar in shape 
to the epithelial cells situated above the columnar cells. They 
also resemble the cells which are situated inside of the epithelial 
lamina. In the larger amplification the nucleus can be readily 

Black 9 has attempted to demonstrate that glands exist in 
the structure and that the cells last mentioned are glands. 
Black lays down as a sine qua non of a gland that there should 
be an opening to the surface. He has made an attempt (Fig. 15) 
to demonstrate such an outlet, but this figure does not show 
clearly that the glands empty into the duct or have an exit at 
the surface. These bodies, however, not only fail (like the 
ductless glands) in this particular, but in more important char- 
acteristics of glands; They do not have (as Robin and Magitot 
remark) a columnar or prismatic cell wall. It is not difficult 
to understand how epithelial cells are scattered in different 
shapes and sizes throughout the peridental membrane. Epi- 

• Dental Cosmos, February, 1809, pages 112-118. 

10 Dental Follicle, page 116. 

11 Embryology, pages 581-90. 


thelial cells have the property of multiplying and developing 
in structures wherever located. 10 

If epithelial cells should migrate within the submucous mem- 
brane and fibrous tissue, proliferation will occur under certain 
circumstances. The tooth, according to Minot, 11 is a papilla 
which projects into the epidermis and, ossifying (calcifying) in 
a particular way, changes into ivory around the soft core or 
pulp; to the papilla the epidermis adds a layer of enamel. The 
tooth proper unites with a small plate of dermal bones at its 
base. By a modification in the jaws the epidermis first grows 
into the dermis and then the dermal tooth papilla is developed. 
The first indication of the development of tooth germs in mam- 
mals is a thickening of the epithelium covering the jaw. This 
thickening, which appears as a ridge during the sixth week of 
embryonic life, forms on the under side of the epithelium. This 
curving ridge expands into an outer portion (the outline of the 
groove between the lip and the gum) and an inner portion, 
the dental shelf which grows obliquely inward. The papilla? 
for the milk teeth are formed on the under side of the shelf, and 
it is thus possible for the shelf to continue growing toward the 
lingual side, so that the second set of germs is developed for 
the permanent teeth. The end of the shelf, toward the articula- 
tion of the jaws, is prolonged without retaining the direct con- 
nection with the epithelium and from this prolongation arise 
the enamel organs for the three permanent molars. Wherever 
a tooth-germ arises the dental shelf is locally enlarged, and the 
local enlargement constitutes an enamel organ which projects 
from the under side of the shelf. The portions of the shelf 
between the enamel organs gradually break up, forming first 
an irregular network, and later separate fragments 1 " which 
may persist throughout life and lead to various pathological 
structures. While the permanent germs are forming, the shelf is 
solid between them, although it has assumed the reticulate 
structure between the germs of the milk teeth. In consequence 
of the reticular formation, the fully developed enamel organs 

Including the epithelial debris of Robin and Magitot. 


have several bands or threads by which they are connected with 
the dental shelf proper. 

After the shelf has developed somewhat, its line of connec- 
tion with the epithelium of the gum becomes marked by a super- 
ficial groove, as may been seen in the human embryo of eight 
to ten weeks. This groove was formerly supposed to be the 
first trace of the dental shelf, but Rose's observations correct 
the supposition. 

The second step in mammals is the formation of outgrowths 
(in man ten in each jaw) from the under side of the dental shelf; 
each outgrowth is the outline of an enamel organ for a milk 
tooth. The outgrowth is covered toward the mesoderm by a 
layer of the epidermis, while the core is filled with polygonal 
cells which resemble those of the middle part of the Malpighian 
layer of the skin. The outgrowths, after penetrating a short 
distance, expand at the lower ends, but remain each connected 
by a narrow neck with the overlying epidermis. The expanded 
end is the enamel germ proper; it very soon assumes a tri- 
angular outline, as seen in sections, owing to the flattening of 
its under side, and at the same time it moves somewhat toward 
the lips. Meanwhile the shelf continues growing on the lingual 
side of each ingrowth to produce the enamel organs destined for 
the second or permanent teeth. 

At this stage it is noticed that the mesenchyma under the 
flattened end of the enamel organ has become more dense, to 
form the outline of the dental papilla, and is beginning to de- 
velop fibrillse around both the enamel germ and the papillary 
outline. The fibrillar envelope is the future dental follicle. 

The third step is a final differentiation of the enamel organ 
and the accompanying shaping of the papilla. The enamel organ 
continues growing and becomes concave on its under side so 
that the mesoderm underneath acquires the shape of the papilla. 
It is now that the form of the tooth is determined by the form 
assumed by the papilla, which in its turn is probably deter- 
mined by the growth of the enamel organ. 

The follicle is merely an envelope of connective tissue in 
which can be distinguished an outer dense and inner looser 
layer; in the latter the cells are more distinct and the fibrillar 



are less numerous than in the former. A rich network of capil- 
lary vessels is developed in the follicle and appears in part as a 
series of villous-like growth into the enamel organ. The folli- 
cle develops first over the lower part of the papilla, then over 
the enamel organ, the neck of which aborts and the follicle 
closes over, completely separating the enamel organ from its 
parent epidermis. The enamel organ changes greatly in appear- 

JFig. 22. — Section through the Incisive Portion of the Lower Jaw of an Ovine 
Embryo, Measuring 82 Millim. (3 1/3 Inches) in Length. Magnified 260 


D, Oral Epithelium. C, Lowest Layer of Cells in the Stratum Malpighii. F, 
Epithelial Cord. K, Bourgeon of the Secondary Cord. I, Follicular Wall. H, Dental 

ance. The layer of cylinder cells is well preserved over the 
concave surface, but only where the epithelium is in contact 
with the dental papilla. In the neck the cells become irregular 
in form. Over the convex surface the cells become lower and 
cuboidal. They ultimately atrophy and flatten out. The cells in 
the center of the enamel organs undergo a peculiar metamor- 
phosis. They remain united together by a few thread-like 

It is obvious from these changes in the embryo how what 
Robin calls the epithelial debris is derived from the epithelial 


cord, the follicular wall and the round bodies of lamina epithe- 
lium debris. According to Ch. Robin and Magitot, 13 who were 
the first to describe these bodies, "The phenomena of budding 
commences, namely, when the epithelial cord has finished its 
course, having conducted the primary enamel organ to that point 
whence its subsequent evolution will be effected and soon after 
the formation of the secondary follicle, immediately after the 
rupture of the cord of the primitive follicle." Robin leans to 
the opinion that these bodies disappear soon after they are 
formed, "The time of their disappearance varies, they remark, 
in different species of animals. In the human embryo the 

Fig. 23.— Vertical Transverse Section through the Incisive Region of the 
Lower Jaw of Human Foetus Measuring 38 Centimetres (15% Inches), 
Magnified 80 Diam., after Drs. Ch. Legros and E. Magitot. 
b, Bony Formation, d, Oral Epithelium, g, Enamel Organs. H, Dental Bulb. 

I, Cord of the Permanent Follicle. K, Debris on the Follicular Wall of the Primitive 

Follicle and from its Cord. K, Epithelial Globule. L, Enamel Organ of the Permanent 


remains of the cord of the primitive follicles may be found, even 
after the formation of the follicles of the permanent teeth, and 
it is probably during the process of eruption that these bud- 
dings become atrophied; in the canine embryo the facts are 
nearly the same; in the bovine and ovine embryos (calf and 
lamb) it has seemed to us that these proliferations disappear at 

13 See their Memoir on the Genesis and Development of the Dental Follicle in Jour, 
de Physiologie de Brown-Sequard, 1860. 



a correspondingly earlier stage ; and we think it safe to say that, 
as a general rule, the complete absorption occurs toward the 
period of eruption. ' ' 

The embryology of the dental shelf, which has been sum- 
marized by Minot from Waldeyer, Kolliker, Von Ebner 14 and 
0. Hertwig, indicates the source of the structures which have 
been mistaken by Black for the limiting walls of glands. 

After the epithelial cords of the temporary and permanent 
sets of teeth have been demarcated from their follicles, the proc- 

: - ■>-.. '-■■■ : --^"--..-:. r :\ : : 

-■3£. ... 

. £*s U 

l< — 

j ^^ /rfaiuufnri) ^^ ; 


Fig. 24.— From the Lower Jaw of an Ovine Embryo, Magnified 80 Diameters, 
Showing the Completed Dental Follicle and the Surrounding Tissues 


a, Meckel's Cartilage, b, Traces of Ossification, c, Lowest Layer of Epithelial 
Cells, d, Oral Epithelium. F, Ameloblastic Layer. F, (Lower) External Layer of 
the Enamel Organ— a continuation of the Layer of Ameloblasts. g, Stellate reticu- 
lum of the Enamel Organ. H, Bulb. I, Follicular Wall. K, Buddings from the 
Cord. B 

ess of cell building proceeds like the process of cord building. 
These buds, according to Charles Robin and Magitot, 15 are given 
off at the upper border of the follicle and below the epithelium 
of the gum. "In fact, as soon as the epithelial lamina loses its 
connection with the follicle, by the rupture of the cord, the epi- 

11 Handbuch der Zahnheilkunde, 1890, pages 209-262. 
1B Loc. cit., 1860. 



tlielial cells composing it become greatly increased in number at 
the severed point. The multiplication of cell-elements results 
in the formation of irregular buddings, which wander in differ- 
ent directions into the deeper portions of the embryonal tissue 
These buddings vary greatly in form; sometimes they are sim- 
ple cylinders, retaining their connection with the primitive 
lamina by pedicles of various lengths, and sometimes this slight 

X 50. One-half-in. obj. No, Oe. 

Fig. 25. — Cross Section of Epithelial Cord. Man. 

I, Peridental Membrane. W, Epithelial Debris or Cord. EO, Endarteritis Obliterans. 

connection is absorbed, thus isolating an epithelial mass." 

This budding occurs at different points along the cord (Fig. 
22) at the end and upon the outer surface of the follicular wall 
(Figs. 23 and 24) at the point where the cord is severed from the 
enamel organ. These gradually diminish as they descend upon 
its sides. Doubtless the epithelial cord remains in the periosteal 


and submucous tissue throughout life. Fig. 25 represents evi- 
dent sections of epithelial cord in a man sixty-eight years of age, 
and Fig. 26 in a dog eight years. In the photographs of the 
scurvy cases and of dogs will be seen evidences of the persist- 
ence of epithelial debris late in life. The position already cited 
from Robin and Magitot as to its early disappearance would 
hence appear to be too strongly taken. 

Robin and Magitot claim that this budding process occurs at 
or about the time of the rupture of the cord. Up to this period 
ossification has not taken place, but then deposits of bone appear 
in the fibrous tissue of the middle and outer surfaces. The bone 
deposit gradually takes the form of the jaw, filling in and 
encroaching upon the fibrous tissue, forming a bony wall on the 
one hand, and the crown and root of the tooth on the other. 
When the tooth is ready to erupt, the crown pushes the soft tis- 
sue laterally, while the root develops, forms a defined wall with 
the peridental membrane between them. The epithelial debris 
(to use their term) which before was scattered over the entire 
surface of the dental follicle, is now crowded into the very nar- 
row space of the peridental membrane, and owing to the position 
of the debris at the upper part of the follicle, it would be nat- 
ural to find most of it at the peridental membrane. 


Development of the alveolar process is relegated to a series 
of cells situated in the fibers of the peridental membrane or 
fibrous tissue, and close to the margin of the bone tissue, and 
throughout the Haversian canals. These cells are called the 
osteoblasts. They perform the function of building up the bone 
tissue. Even after the alveolar process has developed its normal 
shape, so unstable is the nervous system which presides over 
these cells at this locality, that at the slightest provocation, 
either local or constitutional, they will continue their process of 
construction. Hence, the frequency of hypertrophy of the proc- 
ess, and in disease the calcification of the peridental membrane. 

On the other side of the membrane, next the root surfaces, 
may be seen other cells which build up and destroy the cemen- 


turn; these are called cementoblasts and cementoclasts. These 
are of little importance in this connection with the study of this 
disease, although they are frequently present and at work when 
inflammation of the membrane occurs. 

There is, however, another class of cells found in the peri- 

X 560. Xo. 2 projection ocular. One-twelfth obj. Zeiss. 

Pig. 26. — Cross Section Epithelial Cord. Dog. 

I, Peridental Membrane. W, Epithelial Debris or Cord. U, Nerve Tissue. 

dental membrane of the utmost importance in this connection, 
the osteoclasts, located in the fibers, and in close proximity to 
the alveolar wall, and around the inner border of the Haversian 
canals. The function of these cells is to tear down irregular 


bone and tooth structure due to unstable nervous tissue, and 
from the slightest irritation. 

The gums, mucous membrane, alveolar process and peri- 
dental membrane, owing to their transient nature, are influenced 
by the slightest irritation. This influence is the result of both 
constitutional and local causes. It consists of an irritation in 
the peripheral nerves which sets the osteoblasts and osteoclasts 
at work to build up or tear down the alveolar process. This in- 
fluence may be only sufficient to stimulate these cells to action 
without inflammation. This is noticed in the advance toward old 
age, in long, lingering debility, in the development of bone, espe- 
cially the tearing down and the building up of the inferior max- 
illary backward. It may be noted in mild or intense inflamma- 
tion of the peridental membrane, due to more acute forms of 
disease, to scurvy, mercurial, lead and iodide poisoning, or to 
local irritation. So sensitive are these structures that in neu- 
rotics and degenerates the slightest irritation produced in the 
physiologic development of the permanent teeth is sufficient to 
start the osteoblasts to building up bone structure, thus pro- 
ducing that pathologic condition called hypertrophy of the alve- 
olar process; one of the most marked evidences of an unstable 
nervous system. 

The breaking down of the tissues by the osteoclasts may be 
induced by as slight a cause. The alveolar process being so thin 
about the teeth, destruction of the entire walls is accomplished 
without difficulty, and in a very short time, thus loosening the 
teeth, which eventually drop out. 

According to Kaufmann 10 the following processes take part 
in the absorption of bone : (a) Lacunar Absorption, (b) Forma- 
tion of Perforating Canals, (c) Disappearance after Prior 
Absorption of Lime (Halisteresis) (Bony Waste) and Osteo- 

"By far the commonest form of bone destruction is by 
lacunar absorption. This process occurs not only under physio- 
logic conditions, but is extraordinarily frequent in pathologic 
states, e. g., in the various types of atrophy. They form on the 

"Pathologisehe Anatomic. 


smooth, superficial surfaces of the bone deep grooves (so-called 
Howship's lacunas) in which lie smaller or greater polynuclear 
cells (osteoclasts, Kolliker) which evidently blend together (Fig. 
27). There are no alterations of the bone substance that would 
indicate a primary line of absorption (Plummer). The con- 
fluence of these lacuna? form larger cavities. 

"The second form of bone absorption, which is occasionally 
met under physiologic conditions, is by means of perforating 
canals (so-called Volkmann canals). Under physiologic condi- 
tions canals occur in varying numbers in the lamella? (general 


Fig. 27. 

a, Bone Trabecular b. Tubercle with Granulation Tissue, c, Broken-down Tissue. 

d, Blood Vessel, e. Osteoclasts. /, Fat Cells, i Kaut'mann.) 

lamella?) which contain vessels (perforating vessels). These are 
often associated with the Haversian canals and gradually pass 
into them, but unlike them, are surrounded with circular lam- 
ella?. Under pathologic conditions the conception of these per- 
forating canals is somewhat widened. On the one hand 
Volkmann 's canals are spoken of when reference is made to the 
vessels or vascular connective tissue penetrating from one 
medullary space in the spongy substance, or from one Haversian 
canal in the compact substance, to another, in such a way that a 
passage is made from one part of the bone to the other; Yolk- 



mann's canals also include irregular ampula-formed dilations 
or cavities (Fig. 28). By confluence of these are produced cav- 
ities or irregularly outlined canals penetrating the bone sub- 
stance. These, if they empty into the medullary space, become 
filled with cells. 



Dl' w 


a, Large Spaces Resulting from Absorption of the Trabecule, b, Decalcified Bone. 
c and d, Decalcified Bone and Atrophied Trabeculse. c, Haversian Canals. (Kauf- 

"Under much rarer conditions, especially in senile marasmic 
osteomalacia and also in that occurring in pregnancy, bone 
absorption takes place after a prior abstraction of lime (haliste- 
resis) and the remaining substance (bone cartilage) is then fur- 


ther dissolved, passing through a temporary fibroid stage. This 
destruction of the decalcified and interfibrillae decomposed bone 
is produced as a rule without osteoclasts. The decalcified border 
zones of the trabecule appear with simple carmine (coloring) or 
by double stains. ' ' 

Viewing the alveolar process, including the gums, peridental 
membrane and periosteum in man's ontogeny as a whole, it will 
be seen that the changes which are going on in apparently nor- 
mal individuals make it an exceedingly transitory structure. 

In connection with what has already been said in regard to 
the transitory nature of the alveolar process, there is another 
factor to be considered which makes it a doubly transitory 

In man's phylogeny, in some of the lower vertebrates 1T there 
is a continuous succession of teeth throughout life. In man's 
ontogeny, it would be strange if he did not retain still further 
evidences of phylogenetic peculiarities in tooth development in 
relation to the alveolar process. 

Man and some of the lower vertebrates have only two sets of 
teeth. "When the first set comes into place, the alveolar process 
builds itself up about the roots to hold the teeth in place. When 
these are to be lost, a low form of inflammation sets up absorp- 
tion of the bone and the teeth are lost. When the second set 
erupt new bone is developed about the roots to hold the second 
set in place. Should man live long enough the second set would 
drop out even though he possessed a normal healthy body. 
This process is atavistic. With all these changes going on in 
man's ontogeny, we again have an exceedingly transitory struc- 
ture. With the phylogenetic and ontogenetic changes, man has 
a doubly transitory structure in the alveolar process. I have 
called this process of bone absorption, osteomalacia or juvenile 
or senile absorption according to the age of the patient. 18 

Transitory structures are more easily involved in disease 
than other structures. How much more quickly then will a 
structure which is doubly transitory become involved in disease? 

"Talbot. Developmental Pathology: A Study in Degenerative Evolution. 
18 Talbot. Pathogeny of Osteomalacia or Senile Atrophy. The Dental Digest. 
August, 1903. 


Mammals (upon whom researches have been conducted by the 
author) demonstrate they are phylogenetically subject to this 
disease and perhaps lower vertebrates, including the reptiles 
under similar circumstances or environment. 

The Alveolar Process as an End Organ. 10 — I have called the 
alveolar process an end organ. My reason for doing this is that 
the tooth, so far as the process and its diseases are concerned, is 
a foreign body. 20 The arteries, vessels of Von Ebner and espe- 
cially the nerves pass through the bony process, in a wavy man- 
ner and stop at the root of the tooth. 

There are other end organs in the body, chief of which are 
the kidneys, the eye and the brain. Physicians claim, and 
rightly, that because these are end organs they are more easily 
involved in disease and are often the determining factors of 
kidney lesions. Alfred C. Croftan says, "It is not surprising 
to find that particularly those organs that are supplied by end 
arteries are chiefly involved, for in them vascular disturbances 
must first produce nutritional derangement. Chief among the 
organs supplied by end arteries are, precisely, the kidneys, the 
retina and the brain, and I think this explains the frequent in- 
volvement of the kidneys, eyes and brain in Bright 's disease. 
The fact that the retina and the brain are often found injured 
before the kidneys, that cases of Bright 's disease run their fatal 
course occasionally with practically no renal changes, but with 
serious apoplectiform brain lesions and retinitis, bears out this 
conception and constitutes a valid argument against the com- 
mon belief that the nephritis is the primary event and the de- 
termining phenomenon of the disease." 

A marked difference exists between the kidney, eye and brain 
as end organs and the alveolar process as an end organ. This 
difference is the important point in the study of interstitial gin- 
givitis. End arteries running into the kidney, eye and brain, 
owing to the soft nature of these tissues, are given a chance to 
expand and recover, permitting, in a measure, the blood to flow 
more easily, thus prolonging the tendency to disease, or allow- 

19 Endarteritis Obliterans. The Dental Digest, October, 1903. 

20 Interstitial Gingivitis or So-called Pyorrhea Alveolaris. The Dental Sum- 
mary, 1903. 


ing the tissues, under favorable conditions to recover. On the 
other hand, blood vessels extending throughout the alveolar 
process in a tortuous manner cannot expand, and as a result, 
blood charged with toxins and subject to cardio-vascular changes 
immediately sets up irritation and inflammation which results in 
dilatation, bone absorption and arterial degeneration. These 
changes, therefore, will occur much earlier in the alveolar proc- 
ess than in other end organs. 

The transitory nature of the alveolar process, especially as 
an end organ, makes it exceedingly sensitive to systemic 
changes and disease. The sensitiveness of this structure to auto- 
toxic states is easily demonstrated as people advance in years. 
At the fifth period of stress (about forty-five and beyond) the 
excretory organs weaken. The toxic elements of the body are 
not carried off as freely as formerly. These circulate in the 
blood and accumulate in the alveolar process, setting up irrita- 
tion and inflammation. Absorption of the alveolar process grad- 
ually takes place. People enjoying apparently good health will, 
as they advance in years, note the absorption of the alveolar 
process and the exposure of the roots of the teeth. How much 
more readily will absorption take place when the function of 
any one of the eliminating organs be involved, such as constipa- 
tion, asthma, skin affections or kidney lesions. 

In addition to the alveolar process being a doubly transitory 
structure it is also an end organ, of a bony nature and the most 
sensitive structure of the human organism, hence any constitu- 
tional disturbance due to disease, drug poisoning or autointoxi- 
cation would more quickly affect it. Sudden changes in temper- 
ature from heat to cold and vice versa, where the organism is 
unable to adjust itself readily, also leave their mark upon the 
very susceptible tissue. 

The study of interstitial gingivitis and its treatment must be 
based upon the phylogeny, ontogeny and peculiar anatomy of 
the structures involved. There are no other structures in the 
human body associated like the jaws, alveolar process and teeth. 
The pathology, therefore, is unique in itself. 

Transitory structures in the body as well as end organs are 
known to be very susceptible to disease and are, as a rule, the 


first to be involved. The alveolar process, being classed as a 
doubly transitory structure as well as an end organ consisting 
of bone, is one of the first, if not the first, structure to register 
systemic changes. 



The foods which enable the body to repair its waste, to build 
up new tissue and to supply the energy, are divisible into four 
classes: the inorganic substances, the fats or hydrocarbons, 
and the starches and sugars, or carbohydrates, and the proteid 
compounds. These divisions are, however, relative, since the 
proteids may contain both hydrocarbons and carbohydrates. 
The inorganic substances, such as water, phosphates, chlorides, 
carbonates, sulphates, etc., enter the body, as a rule, under their 
own form, either alone or in combination with other classes. 
They are not oxidized or split up within the system to enter into 
the chemical formations of other compounds, but are united 
mechanically with the proteid group. These bodies act, as a rule, 
in a purely mechanical manner. After having served their pur- 
pose, they pass out of the system with the excretions, compara- 
tively unchanged in their composition. They are the only 
member of the group of foods which are of a special interest in 
the present research. The inorganic salts have not received the 
attention from physiologic chemists that their importance de- 
mands. They are, as a rule, found in greater or lesser quanti- 
ties in all foods taken into the body. They do not serve as a 
source of energy, but as the other foods are needed for the de- 
velopment of the tissues, so the inorganic salts are needed for 
the building of bone tissue and the repair of waste. This is ac- 
complished by the soluble salts in the blood. Human blood has 
the following composition : 


Man. Woman. 

25 Years. 30 Years. 

Water 788.71 .... 824.55 

Solids 211-29 .... 175.45 

Proteids and Extractives 191.78 157.93 

Fibrin 3.93 .... 1.91 

Haematin (and iron) 7.70 .... 6.99 

Salts 7.88 .... 8.62 



Blood Corpuscles. 

Blood Plasma. 

CI 1.75 CI 3.536 

K 20 3.091 K 20 0.314 

NA 20 0.470 NA 20 3.410 

SO s 0.061 S0 3 0.129 

P 205 1.355 P 205 0.145 

CaO CaO 

M fln M qn 

These acids and bases exist, of course, in the plasma and the 
corpuscles as salts. It is not possible to determine exactly how 
they are combined as salts, but Schmidt suggests the following 
combination : 


Potassium Sulphate 0.132 

Potassium Chloride 3.679 

Potassium Phosphate 2.343 

Sodium Phospate 0.633 

Sodium Carbonate 0.341 

Calcium Phosphate 0.094 

Magnesium Phosphate 0.060 


Potassium Sulphate , 0.281 

Potassium Chloride 0.359 

Sodium Chloride 5.546 

Sodium Phosphate 0.271 

Sodium Carbonate 1.532 

Calcium Phosphate 0.298 

Magnesium Phosphate 0.218 

It will be seen that the corpuscle contains an excess of 
potassium salts, and the plasma contains an excess of sodium 
salts. All parts of the blood contain salts, however. 

Throughout the entire body, there is a rich supply of blood 
vessels penetrating every tissue. The plasma of the blood pass- 
ing by exosmosis through the walls of the capillaries is thus 
brought in immediate contact with the tissues to which it brings 
nourishment and oxygen of the blood, and from which it 
removes the waste products of metabolism. Other usable prod- 
ucts or lymph are collected in small capillary spaces, which in 


turn open into definite lymphatic vessels. These vessels unite 
into larger and larger ones, which eventually pour this usable 
waste product into the great thoracic or left lymphatic ducts, and 
a second smaller right lymphatic duct. These in turn empty 
into blood vessels, each upon its own side. The lymph contains 
essentially the same constituents as the blood plasma, and the 
salts are found in the same proportion as in it. They are then 
eliminated through the sweat glands, tonsils, mucous glands, 
kidneys, large intestines and salivary glands. 

The composition of the deposits in the various parts of the 
body vary according to the locality and the character of the 
excreta eliminated in connection with them. 

The chemical composition of the human bile, according to 
Jacobson, 1 is as follows: 

Water 977.40 

Sodium Glyeoeholate 9.94 

Cholesterin 0.54 

Free Fat 0.10 

Sodium palmitate and sterrate 1.26 

Leeitine 0.04 

Other organic matter 2.26 

Sodium chloride 5.45 

Potassium chloride . 28 

Sodium phosphate 1. 33 

Lime phosphate . 37 

Sodium carbonate . 93 

Of this analysis the solid ingredients constitute 22.5 parts per 
thousand, of which two-thirds are organic and one-third inor- 
ganic. The inorganic salts of the bile are in most cases returned 
to the blood, where they are redistributed to the tissues. Occa- 
sionally, however, gall stones occur, which are composed of 
(analysis H. D. Geddings 2 ) : 

Moisture 3 .32 

Biliary matter 32 . 182 

Cholesterin 54 . 952 

Matter soluhle in ether 7.77 

Iron traces 

Phosphoric acid traces 

Lime traces 

Magnesium traces 

1 American System of Dentistry. 

2 Transactions South Carolina Medical Association, 1880. 


Secretions of the pancreatic juice (dog) by C. Schmidt are as 
follows : 

Water 900.76 

Solids 99.24 

Organic substances 90. -ii 

Ash S.80 

Sodium carbonate 0.58 

Sodium chloride 7.35 

Calcium magnesium and sodium phosphate 0.53 

The composition of the normal human pancreatic juice has 
not been determined completely owing- to the difficulty of obtain- 
ing the secretion. According to Zawadsky the composition of 
the secretion o\' a young woman was as follows: 

Water iu 1.000 parts 864.05 

Organic substance in 1,000 parts 132.51 

Proteids in 1.000 parts 92.05 

Salts in 1.000 parts 3.4-1 


"Of the inorganic salts, NaCl is by far the most abundant; 
it occurs in quantities varying from 2 to 3.5 parts per thousand. 
The elements of the sweat which are of importance from an 
excretory standpoint are water, inorganic salts and urea or re- 
lated nitrogenous compounds." 

Inorganic salts from the faeces are made up of the salts of 
sodium, potassium, calcium, magnesium and iron. According to 
Enderlin 3 the following represent the composition of the ma- 
terial matter in the faeces : 


Sodium phosphate 2 . 63 

Sodium chloride and sulphate 1.37 


Earth phosphate SO . 37 

Ferric phosphate 2 . 09 

Calcium sulphate 4.53 

Silicic arid 7.94 

Like other constituents of the lymph, the salts vary consider- 
ately in proportion, according as the fluid is more or less rich in 

8 Gamgee, Physiologies] Chemistry of the Animal Body. 
'American Text-Book of Physiology. 


water. The salts are much more abundant than the organic 

Inorganic salts in the urine consist, according to Howell, 4 
chiefly of chlorides, phosphates and sulphates of the alkalies and 
the alkaline earths. As a rule they arise partly from the salts 
ingested with the food, which salts are eliminated from the blood 
by the kidney in the water secretion, and in part they are formed 
in the destructive metabolism which takes place in the body, 
particularly that involving the proteids. Sodium chloride occurs 
in the largest quantities (about 15 grams per day), of which the 
greater part is derived directly from the salt taken in the food. 
The phosphates occur in combination with Ca and Mg, but chiefly 
as acid phosphates, of Na or K. The acid reaction of the urine 
is caused by these latter. The phosphates are produced in part 
from destruction of phosphorous-containing tissues in the body, 
but chiefly proceed from phosphates in the food. Following are 
the average quantities in grams of the chief substances normally 
excreted in the urine in six hours: 5 

Water 1440 —1500 

Solids 57 — 68 

Organic : 

Urea 28 — 68 

Uric acid 7 

Hippnric acid 3 — 2 

Kreatinin 1.7— 2.1 

Inorganic : 

Sodium chloride 15 — 20 

Phosphoric acid 2.5 — - 3 

Sulphuric acid 2 — 2.5 

Sodium 5 — 7 

Magnesium .04 

Potassium 3 — 4 

Calcium 03 

Urinary calculi (classified according to their principal ingre- 
dients), are divided into: 

1. Uric stone, composed of uric acid and acid urates. 

2. Oxalic stone, composed of lime oxalate. 

3. Phosphoric stone, which are composed of magnesium 
phosphate and carbonate with urate of ammonia. 

Landolt, Physiology. 


Each one of these compounds is nearly in a pure state. A 
stone may be composed entirely of one salt or it may be com- 
posed of two, three or four, each compound forming separate 
consecutive layers through the stone. One examination made by 
Howship Dickinson 6 showed eighty-nine per cent lime carbonate 
and the rest lime oxalate and phosphate of lime. 

The deposits upon the teeth are derived partly from the salts 
ingested with foods, which salts are eliminated from the blood in 
water secretion, and in part they are found in the waste of tissue 
which takes place in the body. 

The saliva, according to Schmidt, is made up of the following: 

Water 991.45 

Organic material 2 . 89 

Inorganic : 

Calcic chloride 4 . 50 

Sodium chloride .... 

Calcic phosphate 1.16 



This material floating in the saliva, together with the epithe- 
lial scales and other extraneous matters, contribute to form what 
is known as tartar. This material collects upon the teeth, and 
according to examinations by Stevenson consists of: 

Soft tartar Hard tartar 

on molars. on lower incisors. 

Water and organic matter 21.48 17.51 

Magnesium phosphate 1.31 1.31 

Calcium phosphate with a litte carbon- 
ate and trace of flourine 77.21 81.18 

100.00 100.00 

Another analysis made by Scheheoetskey resulted thus : 

Water and organic matter 22 . 07 

Magnesium phosphate 1.07 

Calcium phosphate 67 . 18 

Calcium cai'honate 8 . 13 

Calcium flouride 1 . 55 


1 Eenal and Urinary Affections. 



Malenfant found that salivary calculi (located in Wharton's 
duct) was composed of: 

Lime phosphate 27 

Magnesium phosphate 1 

Basic lime phosphate 60 

Alcohol and muriatic acid 4 

Ptyalin 2 

Loss 6 


The following are results of analysis of salivary calculi by 
various observers : 

Calcium carbonate 

Calcium phosphate 

Magnesium phosphate. 

Soluble solids 

Organic matter 

Water and loss 

























Deposits in the tissues in gout are made up of soda and lime 
urates. In order to compare the calcic deposits in other parts of 
the body with the so-called serumal deposits upon the teeth af- 
fected with interstitial gingivitis, thousands of teeth were ob- 
tained from three dental offices which make a practice of extract- 
ing teeth. From these one thousand were selected at two differ- 
ent times, making two thousand teeth containing deposits direct 
from the tissues. These were submitted to a chemical analysis 
by J. H. Salisbury, at Rush Medical College, who reports as 
follows : 

"The method which I employed in analysis of calcic deposits 
was as follows : The material was so selected as to be free as 
possible from salivary tartar and a weighed portion was dried at 
100° C. This was then carefully incinerated and again weighed, 
and the difference calculated as organic matter. The residue 
after incineration was divided into two portions, A and B. 

"A was used for the estimation of phosphates as follows: 
The ash was dissolved in nitric acid and the solution precipitated 


with ammonium inolybdate. The precipitate was washed, dis- 
solved in ammonia precipitated by magnesia mixture and the 
precipitate of ammonia magnesium phosphate, washed, dried, 
ignited and weighed. 

"In B, calcium and magnesium were estimated as follows: 
The ash was dissolved in hydrochloric acid and the acid just 
neutralized with ammonia water and sodium acetate added. It 
was then made slightly acid with a drop of hydrochloric acid 
and precipitated with ammonium oxalate. The precipitate of 
calcium oxalate was filtered off, washed, converted into calcium 
oxide and weighed. The nitrate was made alkaline, sodium 
phosphate added, and the precipitate of magnesium-ammonium 
phosphate collected, washed, dried, ignited and weighed. In 
case the phosphoric acid determined in A did not saturate the 
calcium and magnesium obtained in B, the excess of base was 
calculated as carbonate. 

"The following is the composition of the calcic deposits on 
the roots of the teeth, according to analysis of April 18, 1898 : 

Water and organic matter 32.24 

Magnesium phosphate .98 

Calcium phosphate 63 . 08 

Calcium carbonate 3.70 

100 . 00 

"Analysis of the calcic deposits on the roots of the teeth 
October 24, 1898, shows it to have the following composition: 

Water 4.48 

Organic matter 27 . 00 

Calcium phosphate 72.73 

Magnesium phosphate 4.91 


The composition of the alveolar process is as follows : 

Organic matter: Gelatine and blood vessels 33.30 

Inorganic matter: 

Calcium phosphate 51.04 

Calcium carbonate 11 . 30 

Calcium flouride 2 . 00 

Magnesium phosphate 1-10 

Sodium oxide and sodium chloride 1-26 



By comparing the tables of the composition of calcic deposits 
upon the roots of teeth with that of the alveolar process, it will 
be observed that there is very little difference. Tartar deposited 
from the salivary glands and calcic deposits upon the roots of 
the teeth must not be confounded since there is little in common 
between them. Tartar is the principal cause of local interstitial 
gingivitis commencing at the gum margin, while calcic deposits 
are the result of interstitial gingivitis and are always located 
upon the root of the tooth at the point of absorption of the 
alveolar process. The amount of calcic salts in the blood is very 
small as compared with the amount deposited upon the roots of 
the teeth and what is lost in the fluids around the teeth. The 
author 7 has stated that the calcic deposit upon the roots of the 
teeth was the absorbed alveolar process and not derived direct 
from the blood as has been suggested. 

While nearly every kind of food taken into the stomach con- 
tains inorganic salts, every excretory organ of the body throws 
out a certain amount of these salts. Some of these organs 
excrete the salts in a pure state, while in others the salts are 
combined with acids or fluids peculiar to that organ. These salts 
differ in composition and quantity on different days, at different 
hours of the same day; differ at different ages of the same per- 
son and differ in persons of like age, on the same diet. No mat- 
ter how careful the chemist may be in analysis, no two results 
will be exactly alike. For this reason, in tartar and calcic deposit 
upon the roots of teeth, two different analyses of the same de- 
posits are cited. It is evident that while slight differences occur 
in the table, these are due chiefly to the character of the secre- 
tions. The kidneys and salivary glands clearly excrete most of 
the waste inorganic salts. 

Since each excretory organ has its part in elimination of 
waste inorganic salts, it is clear that if one organ becomes tired 
or diseased, other organs have an extra amount of material to 
excrete. In any event, the blood becomes surcharged with waste 
inorganic salts. There is a class of patients with deformed jaws 
and irregular teeth, tonsil hypertrophy, mucous membrane, 
nasal bone and post-nasal space disorder, adenoids, arrest of the 

Endarteritis Obliterans, The Dental Digest, 1903. 


facial bones. They are neurotics and possess degenerate struc- 
tures. This class comprehends those whose nervous system is 
unstable and whose physical development is a departure from 
the race type. This unstable or tired condition may affect but 
one excretory organ. In most cases it affects all organs as well 
as the entire body. In these patients, especially in youth, does 
hypertrophy of the alveolar process take place and large de- 
posits are observed upon the teeth. In this class may be placed 
rachitic children. 

Inorganic salts taken in food are generally utilized until the 
osseous system has attained its growth. This usually occurs at 
about the twenty-sixth year, but full growth may not be attained 
until the thirty-sixth year. When this period has been reached, 
although the body still has the same supply of inorganic salts, 
the system can assimilate only what it needs. The remainder 
becomes waste. Under such conditions the blood is overcharged 
with these salts. 

A condition of the system, which has received too little atten- 
tion, occurs in a class of children ranging from six to eight 
years, who excrete larger quantities of inorganic salts through 
the kidneys and salivary glands. In such cases the teeth 
become coated with tartar. The gums become inflamed from 
irritation. Interstitial gingivitis is developed in youth. These 
children may be rachitic, or border upon the disease. They are 
neurotics, with degenerate structures, suffer from rachitis, rapid 
decay of the teeth and irregularities. They occur in American 
and European schools of idiocy and for dependent and defective 
children. From seventy-five to ninety per cent of these children 
have interstitial gingivitis, ranging from simple inflammation of 
the gums to absorption of the gums and alveolar process with 
pus exudate. Miller noticed in an examination of twenty-six 
cases of rachitic children under twelve years of age that seven 
manifested pronounced symptoms of interstitial gingivitis. 
This was no doubt due to accumulation of calcic salts upon the 
teeth, producing irritation and absorption of the alveolar proc- 
ess and contraction of the gums. 

In cases where large collections of tartar are deposited upon 
the teeth of children there is also an excess of excreta through 


the kidneys. Examination of urine in such cases will reveal 
always from four to eight times more deposit than the normal 
for the age of the patient. Defective nutrition is the result, the 
bones are small, and the jaws and teeth are irregular. The teeth 
decay early in life and it is with difficulty that the decay can be 
arrested. What is true of children is also true of people at 
advanced age. 

After the skeleton had attained its growth (even in those 
cases where no deposits were before observed) the blood became 
overcharged with lime salts and the teeth became a nidus for the 
deposit from the salivary glands. It is, therefore, clear why 
deposits and inflammation of the gums are so common after the 
twenty-sixth year, and more common later in life. Defective 
children and people who have obtained their growth are more 
susceptible to trophic disorders of nutrition and the tissues take 
on disease more readily than healthy individuals earlier in life. 
When inflammation takes place in connective tissue in all parts 
of the body (especially if the blood be surcharged with inorganic 
salts) deposits take place in that tissue through the capillary 
system. On the other hand, when inflammation of the connective 
tissue takes place, if inorganic salts be scarce in the blood, de- 
posits do not take place. As is elsewhere shown, 8 calcic deposits 
on the roots of teeth are a result of inflammation and pus infec- 
tion and not the cause. 

International Dental Journal, April, 1896. 



The etiology of interstitial gingivitis, according to the views 
summarized previously, is divisible into local and constitutional. 
While one school leans largely to the local etiology, another ad- 
vocates as strongly the constitutional theory, and a third be- 
lieves in both the constitutional and local theories as causes. 
The author, from his elaborate researches which began in 1886, 
is an exponent of the latter class. In a general way, etiology may 
be divided into exciting and predisposing. Etiology may also 
depend upon an element dependent on the exciting cause. 
an element dependent on the constitution of the individual at- 
tacked, and finally an element dependent on his condition 
when attacked, both as regards his general system or any one 
of his organs. The chief constitutional causes to which the 
disease has been ascribed are general conditions of the 
health, heredity, constitutional disorders, excessive lime salt 
secretion, meat-eating, nervous exhaustion, scorbutus and uric 
acid states, as well as environment. To these may be added 
drag and metal poisoning such as mercury, lead, brass, 
arsenic, bromides, etc., as well as autointoxication. The local 
causes assigned are acute inflammation of the mucous mem- 
branes, catarrhal states, germs or fungi, irregular teeth, 
lactic acid, pocket disease, hemorrhagic deposits, serumal 
calculi and uncleanliness. That all these factors exercise an 
influence is undeniable, but the enormous etiologic role which 
has been assigned to some of them is the result of generalization 
from too few causes. Many of the assigned causes could be com- 
pressed into fewer etiologic influences. Thus meat-eating, the 
uric acid states, arthritis or gout are too intimately connected to 
be regarded as different causes, from a constitutional stand- 
point. As has been already pointed out, uric acid acts, when it 
acts at all. like lactic and other acids, as a local irritant rather 


than as tho constitutional condition (as many suppose) which 
underlies its production and of which it serves as an index. 

Scorbutus is an expression of a nutritional disorder due very 
frequently in the adult to an excess of meat or a monotony of 
diet. It is a constitutional disorder, peculiarly apt to have its 
local expression in the gums long ere the general constitutional 
symptoms are manifest. The germs and fungi etiologists, on the 
other hand, tend to ignore the constitutional state behind the 
local culture medium, which must be furnished before growth of 
the germ or fungus can occur. In order, therefore, to determine 
whether an alleged cause be exciting or predisposing and what 
is the influence of the etiologic moment, as the union at one time 
of the two constitutional factors already cited is called, analysis 
is required of all the varied factors charged with producing the 
disease. The influence of heredity is generally left out of con- 
sideration unless it be direct, which it rarely is, since heredity, 
as has been well remarked, is usually a prophecy rather than a 
destiny. It hence constitutes, as a rule, a predisposition. 

The chief tissues concerned in the elimination of waste prod- 
ucts are the skin, the lungs and air passages, including the 
mouth and nose, the kidneys, liver and intestines. Interference 
with the eliminatory powers of the kidneys, liver and intestines 
causes autointoxication and is especially apt to throw extra work 
on the skin, lungs and air passages. Of this a sour-winey odor 
of the breath in diabetes is an excellent illustration. What is 
true of such a marked form of sulfoxidation, resulting in auto- 
intoxication, is true of less pronounced forms. The peculiarly 
foul odor of the breath and skin in faecal intoxication indicates 
that the mucous membranes of the nose, throat, mouth and gums 
are doing the work of elimination which should have been done 
by the intestines. The failure of the kidney to perform its share 
of eliminatory work is most apt, however, to find expression in 
the skin, lungs, nose, mouth and gums. 

The influence of the nervous system on the growth and 
repair of any tissue is admitted by every physiologist. This 
influence is entitled the trophic function of nerves. It is not, 
however, exactly settled whether it be exerted through the 
nerves themselves or secondarily through their control of the 


vaso-motor (blood vessel) system. Many trophic disturbances, 
as J. Collins x remarks, are probably due to vaso-motor changes, 
and it is not possible to separate by any sharply defined line the 
vaso-motor from the tropho-neuroses. At the same time, it 
should be distinctly remembered that there exist tropho-neuroses 
in which there are no appreciable vaso-motor changes as in many 
cases of acromegaly and hypertrophies. On the other hand, 
there are any amount of vaso-motor disturbance which are by 
no means trophic in character. Trophic disturbance, which may 
play a very important part at the onset of interstitial gingivitis, 
is neurotic oedema due to nerve irritation. "While this is most 
frequent on the face, lips, tongue, pharynx, forehead and genital 
organs, it also appears on the gums. The cedema reaches its full 
development in from one-half to two hours. There is a feeling 
of stiffness and unyieldingness, but no sensation of inflammatory 
swelling. This type of trophic disorder often initiates changes 
in the mucous membrane which may readily form the basis of 
interstitial gingivitis. This condition may not be only due to 
ordinary nervous causes, but may arise from constitutional con- 
ditions, gout, etc., and toxic influences. 

Nervous Diseases, by Dr. F. X. Dercum. 



Uric acid was first isolated by Scheele in 1776. It consists of 
a white spongy powder. It is devoid of taste and odor. Under 
the microscope it is seen as rhombic tables or as elongated plates 
resembling sheaves or rozettes. As deposited in the urine, it has 
a more or less reddish tinge due to the presence of urinary color- 
ing matter. 

The nitrogenous constituents of urinary excretion consisl 
chiefly of urea or uric acid in certain animals and other nitro- 
genous urinary constituents. 1 

Uric acid is found abundantly in the urine of the lower ver- 
tebrates, such as reptiles, birds and mammals. It would be 
strange if it were not found in the fish tribe. It is more abun- 
dant in birds than in reptiles. It seems to be a normal constit- 
uent in both. Uric acid occurs more frequently in the urine of 
carnivorous mammals, although frequently absent. While found 
in the urine of the herbivora, the quantity is often small and 
variable. Traces of uric acid are found in the organs of these 
animals such as the brain, heart, lungs, spleen, pancreas, while 
it is always found in the blood of birds. In birds, the uric acid 
is partly formed from the purin bases. It would be strange, 
therefore, if it did not develop in man since he has retained 
many of the phylogenetic peculiarities of his precursors. In 
human urine, uric acid is observed in variable amounts. It has 
been observed in healthy human blood. According to Hammar- 
sten, 1 the amount of uric acid eliminated with human urine varies 
considerable but amounts on an average to 0.7 grams per day. 

Hammarsten says, "We used to ascribe an increasing action 
upon the elimination of uric acid to proteid food, but the investi- 
gations of Hirschfeld, Rosenfeld and Orgler, Silven, Burian and 
Schur and others have positively proven that a diet rich in pro- 

Hammarsten, Physiological Chemistry, page 485. 


teid does not itself increase the elimination of uric acid but only 
according to the amount of nucleins or purin bodies contained 
therein. The common statement that the elimination of uric acid 
is smaller with a vegetable diet than with an animal diet, when 
the quantity may be two grams or more per twenty -four hours, 
is explained by this." We would naturally expect to find uric 
acid in patients who live on a strictly vegetable diet as well as 
in those who live on a meat diet, since uric acid is found in herbi- 
vora as well as carnivora. 

The uric acid, in so far as it is produced from nuclein bases, 
is, in part, derived from the nucleins of the destroyed cells of the 
body and in part from the nucleins of free purin bases intro- 
duced with the food. 

Belonging to the same group as uric acid are hypoxanthin, 
xanthin, guauin and adenin. These are called purin bodies and 
are liberated during the digestion of nucleo-proteids contained 
in food. It has been found that a diet of meat, especially veal, 
liver, pancreas and sweetbreads containing a large amount of 
nucleo-proteid, leads to an increase in the excretion of purin 
bodies in the urine as compared with a diet of eggs, butter, milk, 
fruit, vegetables, cheese and bread. The amount of uric acid ex- 
creted in new born infants is in excess as compared with the 

The morbid conditions, in which the uric acid passed in the 
urine is increased, are leucocytosis and leukaemia. This increase 
may be attributed to the degeneration of the excess of leucocytes 
in the blood. Certain drugs increase the amount of uric acid, 
e. g., pilocarpin and salicylates. 

Luxury and modern degeneracy are generally charged with 
the production of diseases which were later found to have at- 
tacked man in prehistoric periods. This has been the case with 
interstitial gingivitis. 

E, B, Andrews expresses the following opinion as to modes 
of life: "I have been led to believe from my own experience 
that this trouble exists largely in the mouths of people accus- 
tomed to luxury— good livers, people about middle age who 
over-eat and under-work." 


No method of living can be regarded as a cause of interstitial 
gingivitis except so far as it affects the general system, thus 
producing trophic changes. There is probably a slight differ- 
ence in liability to interstitial gingivitis between people of seden- 
tary habits and active outdoor workers, as well as between ani- 
mals domesticated or in captivity and those which run at large. 

It is, however, obvious from the data of the chapter upon 
"History" that all races and stations, regardless of time, cli- 
mate, or mode of life, have suffered with the disease. Examina- 
tions of animals in the American and European zoological gar- 
dens show that it is not confined to any class of animals. Dogs, 
cats, horses, cows, whether housed or running at large, suffer 
with it as age advances. 

Uric acid formation is not confined to large eaters. Spare 
eaters may have considerable quantities since they may be unable 
to take care of the uric acid derived from the moderate amount 
of uric acid forming substances (purin bodies) in a normal diet. 

To summarize then, it will be seen that the age of the patient, 
the condition of his system, the character and quantity of food 
eaten and certain drugs must always be considered in relation to 
the quantity of uric acid excreted. 

Since the discovery of uric acid in the urine by Scheele in 
1776, the alleged influence of this factor was steadily advanced 
to the time of Haig, of London, the most prominent exponent of 
this theory. Since his time, a better knowledge of uric acid for- 
mation and its influence upon the system has revealed the usual 
exaggeration of the influence of this particular etiologic ele- 
ment. Researches have shown that uric acid poisoning, in a 
greater or lesser degree, is dependent upon the state of the sys- 
tem, the nature and strength of the exciting cause. All three 
play a part in the digestion, assimilation and elimination of the 
purin bodies which underlie the condition of health formerly at- 
tributed exclusively to uric acid. 

The uric acid theory of disease having been so strongly advo- 
cated by certain physicians, a number of dentists have applied 
the same theory as a cause of interstitial gingivitis and pyor 
rho?a alveolaris. 


What John Fitzgerald 2 calls the gingival organs, possess, as 
he remarks, in common with some other tissues of the body, the 
power of selecting and excreting poisonous substances from the 
blood. Some of these cause hyperemia, or even inflammation, in 
their passage. Uric acid has been found to play a part in so 
many excretions that it has naturally attracted attention here. 
The trend of medical opinion has set strongly in this direction, 
but of late this trend is changing. 

During the past two decades uric acid has assumed again the 
prominence in pathogeny which it once had when called sup- 
pressed gout. It is not surprising, therefore, to find that Reeves, 
Pierce, Rhein and others claim a uric acid etiology for inter- 
stitial gingivitis. In support of this claim are advanced the 
results of three experiments which Pierce has had made on 
tooth deposits. These deposits were examined chemically by 
Ernst Congdon, of the Drexel Institute. 3 The first specimen 
contained a number of needle crystals of calcium urate, a few 
crystals of free uric acid and crystals of calcium phosphate. 
Destructive distillation gave a strong amnionic reaction. The 
murexid test for uric acid and its compounds gave faint results, 
although its characteristic color was evident in several places. 
The second specimen presented the same crystals. The reaction 
to the murexid test was strong and resulted in a number of 
purplish-red spots. Similar results were obtained from the third 
specimen. A. B. Brubaker examined six or eight specimens 
in Pierce's presence, with like results to those obtained in the 
previous examination. In three an abundance of sodium urate 
crystals were present. 

The great deficiency in the experiments thus described is the 
small number of cases examined and the lack of proper control 
experiments. These elements have so frequently led to errors in 
dental pathology that I determined upon a series of investiga- 
tions in two different laboratories, whose results were reported 
some years ago. 4 The Columbus Medical Laboratory was se- 
lected for one series of experiments in special cases. The labora- 

2 The Clinical Journal, March 1, 1899. 

3 International Dental Journal, Vol. XV, pages 1, 217, 501. 

1 Dental Cosmos, April. 1896, page 310. Journal of the American Medical Asso- 
ciation, January 16, 1897. 


tory of the Northwestern University Woman's Medical School 
was selected for the other series of experiments, to which teeth 
were sent as soon as they were obtained. One hundred and fifteen 
teeth were sent to the laboratory last named from three institu- 
tions in Chicago which make a specialty of extraction. These 
teeth had no history other than the fact that the cases were well- 
marked instances of interstitial gingivitis with plenty of calcic 
deposits, and that the teeth were loose in the sockets when ex- 
tracted. Of the one hundred examinations made in the Columbus 
Medical Laboratory, fifty were upon specimens of calcic deposits 
from my patients and fifty were upon specimens obtained from 
the institutions just mentioned, and were therefore without his- 
tory. The tests employed were the hydrochloric acid, the dry 
distillation, and the murexid, these being the tests recommended 
by Pierce. The examinations in the Columbus Medical Labora- 
tory were made by J. A. Wesener, and those in the laboratory of 
the Northwestern University Woman's Medical School by J. H. 

Of the one hundred and fifteen examinations made at the 
Northwestern University Woman's Medical School by the first 
test, in only two cases were found the needle-shaped crystals, 
and one in which there was a slight resemblance of uric-acid 
crystals. By the dry distillation test, thirteen gave no reaction 
from ammonia, and in seven the reaction was slight. The re- 
maining eighty gave a decided reaction. By the murexid test, 
four gave a slight murexid color, but remainder gave no reac- 
tion. Special examinations was made of twelve of these teeth by 
the addition of strong hydrochloric acid, warming, decanting the 
acid, and washing with water. These gave no reaction by the 
dry distillation for ammonia. Two gave a slight reaction by the 
murexid test. In examination of the teeth of three uric-acid 
diathetic women, over forty years of age, uric acid was not 
detectible either by the murexid test or microscopically. The 
examinations made in the Columbus Medical Laboratory were 
still more interesting, since among them were specimens from 
patients whose history could be obtained. Of the fifty obtained 
outside, eight gave positive results from all three tests. The 
other forty-two were positive by dry distillation, and negative by 


the murexid and microscopical tests. Of the fifty patients, 
thirty-eight females and twelve males, thirty-two were over forty 
years of age, twelve over thirty years, and six over fifteen years. 
Twenty-six have uric acid to a greater or less extent, nine 
suffer with indigestion, seven of which are subject to sick head- 
ache, thirty-four have rheumatism. Six are English, and four of 
these have the true gout; the other two have rheumatism. 

All are positive with the dry distillation test. All are nega- 
tive with the murexid test. Forty-nine are negative with the 
microscopical test. One shows needle-shaped crystals, but not 
uric acid. It is a singular fact that in both laboratories, the 
cases in which there were uric acid and gouty histories gave neg- 
ative results. By the dry distillation test, out of two hundred 
and fifteen cases, all but twelve cases (which have been treated 
to remove nitrogenous material) responded. The twelve cases so 
treated did not respond, since nitrogenous compounds in and 
about teeth (even the saliva) burned to an ash will produce 
ammonia. By the murexid test only twelve out of the two 
hundred and fifteen gave a positive reaction. By the micro- 
scopic examination but ten showed crystals. One of the chemists 
who made the examination is positive that they were uric acid 
crystals. The other is not, since lime-phosphate crystals resem- 
ble uric acid crystals too minutely to be distinguished positively. 
For three years Wesener made further examinations as to the 
relative value of the three tests employed. According to his 
experiments the murexid test is the most valuable, the crystal 
test second, and the dry distillation third. The murexid test is 
the most reliable in testing tartar for uric acid, since its red color 
is easily distinguished from other colors and the test is simple in 
application. The test for crystallized uric acid is very unsatis- 
factory, since here must be dealt with a complex mass which not 
only contains crystals of calcium phosphate (very similar to 
those of uric acid) but a great mass of detritus obscuring the 
crystals of uric acid. If crystals be present they by no means 
settle the existence of uric acid. When the faintest quantity pos- 
sible of uric acid is mixed with tartar from teeth and subjected 
to crystallization, the results are always negative. If subjected 


to the murexid test, the results are always positive. The dry 
distillation test is so inaccurate as to be unworthy consideration. 

Since these results were published, seven hundred and thirty- 
five cases have been examined. These examinations were con- 
ducted by Jerome H. Salisbury, now of Rush Medical College. 
The teeth procured from institutions which make a specialty of 
extracting contained the dark calcic deposit above the pus line. 
By the murexid test, six out of the three hundred gave a distinct 
reaction; eighteen showed crystals under the microscope. The 
murexid test was performed as follows : The deposit was se- 
lected as carefully as possible, removed from the tooth, and 
placed in a small porcelain crucible. A drop of pure nitric acid 
was added and the mixture evaporated on the water bath. When 
dry, the evaporation was repeated with another drop of nitric 
acid, and the crucible allowed to cool. When cool, the color pro- 
duced by the nitric acid was observed, and then a glass rod, wet 
with ammonia water, was brought near the deposit, and any color 
produced was noted. If no color was observed, the ammonia was 
allowed to flow over the residue. A yellow color was produced 
in many cases by the nitric acid, which was deepened by the 
addition of ammonia. The microscopic examination was made 
by scraping off the deposit and evaporating it with a drop of 
hydrochloric acid. The residue was moistened with water, and 
the insoluble material placed on a slide and covered with a 
cover-glass. It was examined with a No. 7 objective. Uric 
acid, therefore, occurred in a certain very small proportion of 
cases of calcic deposit on the teeth. 

Four hundred and thirty-five cases were later examined, mak- 
ing in all nine hundred and fifty. Out of these four hundred 
and thirty-five cases only four per cent showed uric acid by the 
murexid test and eight per cent by the crystal test. Since the 
crystal test is not so accurate as the murexid test, it is safe to say 
that six per cent was the actual per cent of uric acid. As a 
result of the different experiments, in the first two hundred and 
fifteen cases five per cent uric acid was found. In the second 
three hundred cases, four per cent, and in the third four hundred 
and thirty-five cases, six per cent was found. In an examination 
of nine hundred and fifty cases by different chemists at different 



periods, five to six per cent give positive results as to uric acid by 
the cliemic and microscopic examination. These results demon- 
strate conclusively that interstitial gingivitis is not due solely to 
uric acid ; that uric acid when found is merely an expression of 
the uric acid diathesis and a coincidence, since it is not always 
present in the gums and tartar of patients attacked either by 
gout or the uric acid diathesis. In the six per cent of cases there 
was nothing to show that uric acid was the cause of interstitial 
gingivitis, since the deposits were examined after the teeth had 
been removed. Any other irritation may have been the exciting- 
cause. Uric acid acts, when at all, solely as a local irritant, like 
other acids and poisons. A microscopic examination of the tis- 
sues involved occasionally reveals uric acid crystals. The fact, 
however, that they are found in a small number of patients suf- 
fering with interstitial gingivitis shows that they cannot be de- 
pended upon as a general cause of the disease. 



The relations of heredity are far more intricate than is usu- 
ally assumed to be the case in the average discussion of the sub- 
ject. The problem consequent on impregnation is not that 
involved in the mere carrying of the mixture of parents in a fully 
developed form through intra-uterine life. As all vertebrate 
organs pass through the same stages before definitely differen- 
tiating, the later types have to gain at the expense of the earlier 
and hence must receive greater energy from the direct ancestors. 
The want of this energy is shown in the various defects and de- 
partures from types which occur in the different degeneracies 
and congenital defects. The types of heredity ordinarily con- 
sidered are direct heredity where the individual takes after im- 
mediate ancestry, and type heredity where he takes after the 
type to which he belongs. 

The influence of heredity in interstitial gingivitis, as in other 
morbid conditions, is still a mooted question. Morbid heredity, 
as I have elsewhere shown, 1 is practically divisible into direct 
and indirect. The first is the direct inheritance of the weakened 
organism of the mother; the second is a condition of intra-uter- 
ine infection. Heredity further should be distinguished from 
congenital states which result from the operation of germs or 
toxins during a particular pregnancy wherein these pass through 
the placenta to the foetus. A child may be born of a tuberculous 
mother with a tendency to tuberculosis but may not develop it ; 
on the other hand the tubercle bacilli may infect it through the 
placenta so that it is born with tuberculosis. 

The weakened organs of the mother (due to an unstable nerv- 
ous system) may cause the child to inherit an unstable nervous 
system. This, in turn, may cause an arrested or excessive devel- 
opment of the jaw and alveolar process in the child at the periods 

Talbot. Degeneracy: Tts Signs, Causes ami Effects. 


of stress. Under such conditions the jaw is most frequently 
arrested. An arrested jaw and alveolar process usually mean an 
irregular dental arch in which the teeth are so closely packed 
(owing to the crowns being straight, not bell-shaped) that the 
alveolar process is almost entirely destroyed between the teeth. 
To keep the gum margins clean and in a healthy condition in such 
a mouth is almost impossible. The slightest inflammation, due 
to irritation, of the gums, peridental membrane or alveolar proc- 
ess, whether local or constitutional, will cause its destruction 
sooner or later in the life of the individual. 

Again, because the alveolar process is a transitory structure 
as well as an end organ, and because of its thinness around the 
teeth, the inheritance of a lowered vitality, both in the individual 
or in the immediate structure under discussion, or both, will fur- 
nish a predisposing cause for interstitial gingivitis. This is why 
so many neurotic and degenerate children possess irregular jaws 
and teeth, and why these children early develop interstitial gin- 
givitis." Hence heredity may well be the indirect cause of inter- 
stitial gingivitis. 

The reported cases of direct heredity in the pyorrhceic stage 
of interstitial gingivitis may belong in one or the other of these 
categories, but such a theory can hardly be considered tenable. 
Researches of many able investigators have failed to demon- 
strate the germ theory, local or inherited, in causal relation to 
interstitial gingivitis, as practiced by specialists, as we shall 
see in Chapter XII. It is known, however, to every specialist 
that the secondary condition of this disease (pyorrhoea alveola- 
ris) is due to germ infection. Pus germs producing the sec- 
ondary stage of the disease, are local in nearly every mouth and 
are not supposed to be inherited. Pus germs in the mouth do 
not, apparently, produce the first stage of the disease (intersti- 
tial gingivitis), which is simple inflammation. We could hardly 
expect to find directly inherited germs from the mother to the 
child causing infection of the gums, peridental membrane or 
alveolar process later in the child's life, since there is a period 
between birth and the eruption of the temporary teeth where 
no alveolar process is present and no infection takes place. 

a Talbot. Developmental Pathology: A Study in Degenerative Evolution. 


Transitory organs are bound to be weakened by heredity, 
both in their structure and in their resistance to morbific germs 
and agencies. These weaknesses are especially apt to be empha- 
sized during the second and third periods of stress', when the 
temporary and permanent teeth are erupting. Such weaknesses 
may be the outcome of general nerve exhaustion on the part of 
the parents (the mother especially) or of the child itself, and 
they represent a changed (transformed) heredity far more com- 
monly than a direct. This heredity may be more intense than the 
constitutional lack of health in the parents. On the other hand, 
the influence of intermarriage of several healthy generations 
may so offset the evil results of the defects in the parents that 
the inheritance of disease or the tendency to disease is slight, 
if at all existing in the child. The last type of heredity, called 
atavism (or "throw-back" by breeders), is more likely to work 
for good than for evil, although disease effects are more gener- 
ally looked for. Concerned in this latter, where the individual 
throws back to immediate remote ancestors, this element of 
atavism tends, through preserving the type, to offset the defects 
of immediate heredity and, indeed, often underlies the apparent 
difference between children of the same parents. It likewise 
prevents equal inheritance from both parents, and sometimes 
favors inheritance of strength or defect from either. It under- 
lies also so-called collateral or indirect heredity and the trans- 
mutation of heredity. By virtue of this atavism, a serious nerv- 
ous defect in a parent or parents might express itself only in 
an increased tendency to disease on the part of the child's tran- 
sitory structures and end organs. 

The periods of stress are times in the life of man when cer- 
tain great life functions are developing or undergoing retrogres- 
sion. These periods of stress are, during development in utero, 
during the first dentition, during the second dentition (often 
as late as the thirteenth year), daring puberty and adolescence 
(fourteen to twenty-five), during the climacteric (forty to sixty), 
when uterine involution occurs in woman and prostatic involu- 
tion in man, and finally, during senility (about sixty and up- 
wards). These periods often constitute a cause for the produc- 

3 Talbot. Developmental Pathology: A Study in Degenerative Evolution. 


tion of disease even though hereditary defect itself be absent 
until this time when it first makes it appearance. 

Another factor to be considered in this connection as compli- 
cating the diagnosis of heredity in interstitial gingivitis is envi- 
ronment, understanding by this term all the external conditions 
that can favor the development of the disorder. Family hab- 
its and surroundings are apt to be alike for every member, so 
that if anything in the environment especially favors the break- 
ing out of a disease in one member, the same cause or causes 
are equally likely to favor the occurrence of the disorder in sev- 
eral members or even generations of the family, and this may 
give rise to a suspicion o\' heredity. This consideration applies 
to interstitial gingivitis, since the disease has been known to 
develop in different members o\' the same family at similar 
periods o\' life and under the same conditions. 

That constitutional conditions of hereditary origin favor the 
occurrence o\' interstitial gingivitis is undeniable, but this does 
not mean that interstitial gingivitis itself is hereditary. They 
favor its occurrence just as they favor any other morbid con- 
dition, by lessening resistance or by preparing the way. The 
interstitial gingivitis is only one ol' the many accidents that are 
thus facilitated. 

So far as salivary concretions are to be regarded as an excit- 
ing cause, heredity may be put out of court, since these (though 
varying widely in different individuals in the amount of the 
deposits, and consequently in the irritation produced) are de- 
pendent upon more remote constitutional or local conditions 
and have no direct connection with the heredity. Thus the vari- 
ous deposits attributed to lithaunia or arthritic conditions (noto- 
riously hereditary), are merely incidental to those conditions 
and not essentially connected with their constitutional origin. 
The constitutional conditions merely happen to furnish the irri- 

Local uric acid poisoning 1 is, as I have elsewhere shown, 
occasionally associated with interstitial gingivitis. The coexist- 
ence signifies the lowered vitality of the system and autointoxi- 
cation, rather than the etiolgy. 

The Dental Cosmos. 1S06. page 312. 


The same is true of al] the other neurotic, rachitic and degen 
erative conditions, hereditary or otherwise, thai are met with, 
associated with gingival inflammation. They favor the occur- 
rence of the disease by causing a weakened capacity of resist- 
ance, thus predisposing to the attack of any irritation. The 
mouth, resistant as it ordinarily is, is at all times open to irri- 
tation and infection. When resistance is impaired it gives way 
at its most vulnerable points, and the gingiva] margin because 
of its transitory and end organ nature is one of these points. 
Interstitial gingivitis is favored or hindered, like other disor- 
ders, by constitutional conditions which may or may qoI be in 
berited, and which hear toward it the relations only of predis 
posing and accessory causes. 

To summarize, therefore, it is reasonable to suggest that 
interstitial gingivitis and pyorrhoea alvoolaris are not inherited. 

Interstitial gingivitis is the primary condition and represents 
the reaction of a weakened transitory end organ to constitu- 
tional or local irritation. 

Heredity, direct and indirect, may of course weaken resist- 
ance and predispose to the disease, particularly in a structure 
so transitory as the alveolar process, hut no direct transmission 
of infection is either demonstrable or even tenable. 

Pyorrhoea alvoolaris is a secondary infection grafted on the 
original inflammation by the agency of local pyorrhceic germs 
such as are prone to invade any exposed membrane, and have 
no relation whatever to heredity. 



One important factor of predisposition to interstitial gingi- 
vitis is degeneracy, either local or general. Three possibilities 
of life await each living being. The individual may remain 
primitive and unchanged, progress toward a higher type or 
retrogress to a lower type. In these three conditions, the fact- 
ors underlying the stable state force the structures to remain 
as they are; those underlying the progressive tendency make 
them more elaborate, while the third tends to simplify structure. 
Degeneracy is a gradual change of structure by which the organ- 
ism becomes adapted to less varied and less complex conditions 
of life. It is a reverse of development which proceeds from the 
indefinite and homogeneous to the definite and heterogeneous 
with a loss of explosive force due to the acquirement of inhibi- 
tions or checks. In proportion to the depth of degeneracy does 
it affect the early simpler or late complicated acquisitions. The 
opposite process of progression is a gradual change of struc- 
tures by which the organism becomes adapted to more varied 
and more complex conditions of life. In progression there is a 
new expression of form corresponding to new perfection of 
work in the animal machine. In degeneracy, there is suppres- 
sion of form corresponding to cessation of work. Elaboration 
of some one organ may be the necessary accompaniment of 
degeneracy in all the others. On the other hand, degeneracy in 
one organ may be the necessary accompaniment to elaboration 
in all the other organs. During any of the periods of stress 
defects due to degeneracy are apt to appear and affect the line 
of least resistance, determined by the depth of degeneracy, as 
well as the variability of the structures concerned. This is the 
reason certain individuals develop disease or become suscepti- 
ble to disease since at these periods the entire organism under- 
goes change, and the organs most affected by degeneracy are the 


first involved. This is particularly true of transitory structures 
like the alveolar proccess and it, in addition to being doubly 
transitory and the most sensitive structure in the body is also 
an end organ like the brain, eye and kidney. The teeth and jaws 
are among the most variable structures in the body, and they 
are peculiarly apt to be affected by either general degeneracy, 
which affects the body as a whole, of local degeneracy, which 
may affect one organ or structure or part of them. Degeneracy 
factors causing nervous exhaustion in the parents leave their 
stamp on the tonicity of the child's organs to combat disease. 
Every nerve cell has two functions, namely : sensation or 
motion and growth which are dependent upon each other, that is, 
if the cell be tired by excessive work along the line of sensation 
or motion, growth later becomes impaired. The cell then not 
only ceases to continue in strength, but becomes self-poisoned. 
Each of the organs (heart, liver, kidneys, etc.) has its own sys- 
tem of nerves (the sympathetic ganglia) which while under the 
control of the spinal cord and brain, act independently. If these 
nerve centers become tired, the organ fails to perform its func- 
tions, the general system becomes both poisoned and ill-fed, and 
nervous exhaustion results. In most cases, however, the brain 
and spinal cord are first exhausted. The nerves of the other 
organs are thus allowed too free play, and exhaust themselves 
later. This systemic nerve exhaustion particularly affects the 
testicle in the male and the uterus and ovaries in the female, 
hence an unstable nervous system in the offspring results. 
Through this, the body is imperfectly supplied with natural 
tonics (antitoxins) formed by these structures, and the general 
nervous exhaustion becomes still more complete. All the organs 
of the body are thus weakened in their function. Practically 
the neurasthenic's organs have taken on degenerative functions 
though not degenerate in structure. Through the influence of 
these various nerve exhaustion agencies, the spinal cord and 
brain lose their phylogenetic gains and the neurasthenic is no 
longer adjusted to environment. Since the reproductive organs 
suffer particularly, children, born after the nervous exhaustion 
in the parents, are more or less checked in development owing 
to the depth of degeneracy and the influence of healthy atavism. 


They have degenerations in the structure of their organs which, 
in the parents were represented by neurasthenic disorder in 
function. As the ovaries of the neurasthenic female generally 
exhibit prominently the effects of nervous exhaustion, the off- 
spring does not retain enough vigor to pass through the normal 
process of growth or should it survive, it is usually affected by 
the profound neuroses. In these instances in connection with 
irregular dental arches, there is always interstitial gingivitis 
and pyorrhoea alveolaris. 

The action of degeneracy, considered as a local factor of con- 
stitutional origin, may be exerted to preserve embryonic con- 
ditions in adult life. Such preservation may result in the break- 
down o\' tissues which would otherwise withstand germs, toxins 
ami poisons, or other causes of disease external to the tissues. 
Given this condition o\' local degeneracy, a local predisposing 
factor is added to both the exciting causes and the constitu- 
tional predisposing factors. So long as the teeth and transi- 
tory structures remain in the comparatively stable condition of 
primitive races, this factor is, to a great extent, in abeyance. 
When, however, the jaw begins to evolve (grow smaller), the 
degenerate types find this factor adding dangers in their phylo- 
geny. In the degenerate, the struggle for existence between 
organs (the brain and skull on the one hand, and the face, jaws 
and teeth on the other) is not properly balanced, whence the 
dangers from these local states of degeneracy that in the higher 
types are expressions of advance undergone without danger. 
This is excellently illustrated in the embryology of the mucous 
membrane. This, in degenerate children, often fails so to de- 
velop that the bactericidal function of mucus does not appear. 
This hereditary feebleness of the mucous membrane is pecu- 
liarly apt to occur in the nose, throat and gums, but other mu- 
cous membranes are not exempt. 

Miller, as elsewhere stated, found a little over thirty-three 
and one-third per cent on examination of twenty-six rachitic 
children under twelve years who manifested interstitial gingi- 
vitis. Considering that most of these manifested symptoms 
of inherited congenital or acquired constitutional defect, such 
a small proportion is rather remarkable. The fact suggests one 


of two explanations — either the children in the institution vis- 
ited by Doctor Miller took better care of their teeth and gums 
than is usual with this class, or the cases in which pus existed 
only were classed as pyorrhoea. I have examined the mouths 
of deaf mutes, blind, idiotic, feeble-minded and rachitic children 
in the institutions in America and Europe. Interstitial gingivi- 
tis was found in all its stages, from simple inflammation of the 
gums to loosening of the teeth, in from twenty-five to seventy- 
five per cent. In these cases not only are there constitutional 
factors, but also uncleanliness of the mouth and gum tissues. 
The degenerate children of even the best families encountered 
in office practice usually have jaw deformities and teeth irregu- 
larities as well as interstitial gingivitis. Patterson has had 
under observation thirty-eight cases of well-marked pyorrhoea, 
thirty-three of which co-existed with nasal catarrh. These 
cases were, no doubt, those of degenerate patients. The nasal 
catarrh was a coincidence dependent on the general deficiency 
of the mucous membrane. 



The causes which produce interstitial gingivitis may be 
divided into those producing infections and those producing irri- 
tations from intoxication. 

The infections may be divided into local and constitutional. 
The constitutional infections are those which infect the gums, 
alveolar process and peridental membrane, through the blood, 
such as tuberculosis, syphilis, scurvy and similar diseases. 

The local infections are those in which the germs infect the 
tissues directly producing anthrax, actinomycosis, gonorrhoea, 
syphilis, apthae, 1 dead pulps and many other diseases for which 
no name has yet been applied. 

All these diseases have constitutional symptoms which are 
associated and which must be understood in making a diagnosis. 
Since most of these infections, whether constitutional or local, 
are special diseases of the gums and alveolar process, they re- 
quire special constitutional treatment according to the general 
symptoms as they arise and are therefore to be placed in a spe- 
cial class by themselves. They are not considered again in this 

Experiments with bacteric infection upon animals and human 
to produce interstitial gingivitis have been made by Galippe, 
Miller, Rhein, Carpenter and Talbot. 

Galippe ~ was probably among the first to make analytic 
experimentation in the bacteriology of this disease. He claims 
that there is found in the pus of pyorrhoea a parasite, resembling 
in shape the Greek letter N. Injecting this into the belly of a 
guinea pig, abscesses resulted, which had a special tendency to 
affect bone tissue. Injections into the space between the teeth 
and gums were negative in result. Galippe regards his experi- 

1 Talbot. Some Bacterial and Non-bacterial Diseases. Journal of the American 
Medical Association, February 10, 1912. 

a Die Infectibse Artbro-Dentaire Gingivitis, 1888. 


ments as suggestions for further research, but not demon- 

Miller, 1 after explaining his own methods, made a series of 
culture experiments on agar-agar at blood temperature. Twelve 
cases of pyorrhoea in human beings, and six in dogs, were exam 
ined. He isolated twenty different bacteria from human beings, 
and nine from dogs. Among the twenty kinds, staphylococcus 
pyogenes aureus was found twice, staphylococcus pyogenes 
albus once, streptococcus pyogenes once. Of the other sixteen, 
nine subcutaneously injected produced no particular reaction, 
four a slight, three a severe suppuration in the subcutaneous 
connective tissue. . . . Among the nine species found in 
dogs, staphylococcus pyogenes albus occurred once. Of the 
other eight, two subcutaneously injected caused no reaction, and 
five but slight, One caused very profuse suppuration, by which 
large portions of skin exfoliated. . . . Microscopic exami- 
nation of stained sections revealed masses of different bacteria, 
cocci and bacilli. Leptothrix occurred infrequently, and then 
only on the surface of the cement, and where there were micro- 
scopical cavities in it. . . . Miller succeeded consequently 
in cultivating a large number of bacteria from pyorrhoea areo- 
laris which possessed pyogenic properties, but was not able to 
determine the constant occurrence of any one which might be 
regarded as the specific micro-organism of pyorrhoea alveolaris. 
Miller remarks that it is not evident from Oalippe's communica- 
tion whether lie found the X or B bacterium in all cases exam 
ined, or but once. 

Sudduth, after repeated examinations, arrived at the same 
conclusion as Miller. 

Dr. M. L. Rhein's 4 investigations are here given. He says, 
"The results of my investigations made at the Pediatric Labora- 
tory in New York some eleven years ago are given here for the 
first time as corroborative evidence that in healthy bodies it is 
impossible to produce this disease. Four guinea pigs, proven 
later at the autopsy to be absolutely free from any taint of dis- 
ease oi" abnormality, were chosen. Their food was carefully re- 

Micro-Organisms of the Human Mouth. 

PyorrhcEa Alveolaris. The Items of Interest. June, 1910. 


duced day by day until they died at the end of ten weeks. Con- 
trol pigs were kept in a cage alongside of these and fed with 
the usual quantities of food. About the beginning of the tenth 
week when the pigs wore weakened from lack of food, all eight 
of them were inoculated in the pericemental regions with injec- 
tions of liquid cultures developed in bouillon, from pus taken 
from the pockets of pyorrhoea! patients. On the third day all 
evidence of the trauma produced by the injections had disap- 
peared. At no time had there been the slightest evidence of 
even a resulting gingivitis. As stated before, the autopsies 
showed all four pigs to have absolutely normal organs, although 
they were practically skeletons. Of the control pigs, while three 
of them showed the same immunity to infection, the fourth one 
showed evidence of inflammation, and at the end of the fifth day 
there was a distinctive serus exudate coming from the neck of 
the front tooth around which the injections had been made. I 
have always regretted the fact that this pig was not killed and 
an autopsy held. 

"Before this time I had. examined the months of many hun- 
dreds of guinea pigs inoculated by the Board of Health with 
tuberculosis. Every one of these showed the most marked evi- 
dence of pyorrhoea! conditions. In the same manner a visit to 
any sanatorium for tuberculosis cases will show on examination 
of the mouths, pyorrhoea alveolaris in a degree of severity 
exaetly conforming to the inroads which the disease has made. 
A like examination of the medical wards of any hospital con- 
taining cases of diseases of the heart, kidneys, liver, lungs, etc.. 
will, if no attention has been paid to prophylaxis of the mouth, 
show conditions of pyorrhoea. Even when the most strenuous 
efforts in this direction of mouth care are taken, if the form of 
the malnutrition has passed to a certain stage, no care of the 
mouth is sufficient to prevent the marked development of pyor- 
rhoea alveolaris." 

The results obtained in the Columbus Memorial Lahoratory 
of Chicago, by W. A. Evans for the author, were as follows: 

In order to determine whether a specific bacterium existed in 
the pyorrhoeic stage of interstitial gingivitis in man (neeessary 
to constitute this stage a special diseased, pus from more than 


fifty cases was examined. In all, the pus was obtained from the 
gums by a platinum needle under proper methods of steriliza- 
tion. The pus from some cases was smeared on a slide. This 
was stained and such determination made as was possible with 
this procedure. "With the pus from fifteen cases, agar was inocu- 
lated and placed in Petrie's dishes. The individual colonics 
were grown on gelatin, agar, bouillon, potato and blood serum. 
The results were as follows: In fifteen cases in which the 
organisms were plated out, fifty-five organisms were found. In 
two there was no growth. Two had but one species of germs, 
two had six, one had seven, and one had ten. The germs found 
are divisible into three classes: Those usually pathogenic to 
man, those exceptionally pathogenic to man, and those never 
pathogenic to man. The first class was found thirty times, the 
second twelve, and the third thirteen. Class third is, no doubt, 
seemingly smaller than it should be, since many members of it 
probably do not grow on ordinary culture media. Of the germs 
most frequent and important, staphylococcus pyogenes aureus 
occurred nine times, staphylococcus pyogenes albus six times, 
and staphylococcus pyogenes citreus once. A lanceolate diplo- 
coccus, growing like pneumonococcus, was found six times. 
Streptococcus pyogenes was found twice. Bacillus coli com- 
mune was found twice. A bacillus growing like the diphtheria 
bacillus occurred twice. This last bacillus had the appearance 
of the Klebs-Loeffler bacillus. It lay on the slide like it and it 
stained irregularly. Of the less important organisms, bacillus 
pyocyanens was found three times, micrococcus tetragenus seven 
times, leptothrix seven times, bacillus mesentericus twice, bacil- 
lus subtilis three times. There was also present a peculiar large 
club-shaped fungus somewhat resembling the degenerative 
forms of actinomycosis. 

Did these examinations stand alone, definite conclusions 
could not be drawn from them. These, however, are admissible 
since all observations on this subject tend in the same direction. 
While, as already stated, Galippe believed that he had isolated 
two bacteria capable of causing pyorrhoea alveolaris, still he 
failed with both to produce the disease. This failure, according 
to the laws of Koch, is fatal to the position taken. 


M. Herzog, of the Chicago Polyclinic, on examination of 
cases of interstitial gingivitis, which had not reached the pyor- 
rhceic stage, had the following results : Pieces from the gum 
margin which had been fixed and hardened in a formalin solu- 
tion, were partly imbedded in celloidin, partly in paraffin. The 
sections were stained according to various methods, including 
Gramm's, eosin (Unna's) and alkaline methylblue stain. The 
examination of the tissue shows an unchanged lining of stratified 
squamous epithelium, and, in the connective tissue below the 
former, well-marked evidences of an inflammatory process. The 
round-cell infiltration is best marked in the deeper layers toward 
the periosteum, while the layers of connective tissue fibers nearer 
to the lining epithelium show less evidences of inflammation and 
are partly entirely free from any round-cell infiltration. The 
infiltrating round cells are of the type of lymphocytes, plasma 
cells and plasma mast cells. Very large and typical mast cells 
are frequently found in the neighborhood of small vessels. 
Many of the vessels seen are quite tortuous, and the vascular 
supply of the connective tissue appears to be considerably in- 
creased beyond the normal. Bacteria could not be demonstrated 
in the inflamed areas. 

M. Herzog 's examination of the interstitial gingivitis, pro- 
duced by mercury in dogs, failed to reveal any bacteria. He was 
of opinion that the histologic changes of inflammatory type 
found, were due to the chemotactic influence of mercury and not 
to microbic action. 

In a paper 5 read before the Section on Stomatology of the 
American Medical Association, at Columbus, Ohio, George T. 
Carpenter mentioned some very interesting experiments in this 
connection. By infecting a fresh wound in the gums of rabbits 
with pyorrhoea and other pus he found the parts will remain 
infected only from two to five days. In other rabbits a rubber 
band was placed around teeth and pressed under the gums until 
inflammation resulted, when the parts were infected with pyor- 
rhoea and pus from a chronic ulcer; pus infection resulted. 

Like experiments were made in the human mouth on gums 

6 Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrl 


which had been neglected as well as on healthy gums, and with 
similar results. His experiments tend to show that, when ani- 
mals and man are healthy, the tissues resist infection ; but when 
diseased, infection results. All yield to treatment. 

On examination of pus taken from pyorrhoea pockets pro- 
ceeding from acute infection, two competent bacteriologists were 
unable to find a micro-organism not found in pus from other 
infected tissues. 

These results, in Carpenter's opinion, tend to show that a 
specific germ, to which pyorrhoea alveolaris is attributable, has 
not yet been found. 

The disease being so prevalent among dogs, it occurred to me 
that they would be of great value for experimental inoculation. 
The prevalence of the disease in dogs suggests that if it were a 
specific infection, these must be inoculable. Miller r ' had made a 
few inoculations of pus as well as of the deposits around the 
teeth. Slight inflammation, and, in one case, a little suppuration 
alone resulted. He afterward isolated twenty different bacteria 
from the human mouth and nine from dogs. Some of the 
uncommon varieties were infective, but without marked results. 
Isolated varieties would probably not produce results that could 
be attained by inoculating animals with the fresh secretion (pus 
and other deposits) from dogs already affected with the disease. 
A dog was procured from the Veterinary Hospital whose gums 
and outer alveolar process were almost entirely absorbed with 
pus exudate. Street dogs selected for inoculation were forty-six 
in number, ranging in age from one year to seven. They were 
of all breeds and conditions. Some were well fed, others very 
thin. Many had sound, healthy gums ; others had slight inflam- 
mation at different localities. No dog was used whose gums 
and alveolar process had become infected or whose tissues were 
absorbed. Two dogs were operated upon at a time. The gum 
was separated from the necks of the teeth down to the alveolar 
process and peridental membrane — one half at the canine, the 
other at the second pre-molar, since in a majority of cases the 
disease began at the canine tooth, probably on account of its 
prominence and the thinness of the alveolar process. The sec- 

Micro-Organisms of the Human Mouth, page 329. 



ond pre-molar was selected because it is the least prominent. 
The secretions about the teeth and gums of the diseased dog 
were collected upon a platinum wire (previously sterilized) and 
conveyed to the injured parts. Thirty-nine healed in eight days. 
In these the gum tissues were healthy. The pus had no effect. 
The wounds healed as rapidly as any wounds possibly could. 
In seven the gums were inflamed and infection occurred. Sup- 
puration was slight in four and considerable in three. The path- 
ologic findings in these cases were not unlike inflammation and 
infection in other tissues. Similar results would, no doubt, have 
taken place if inoculation had been performed with pus from an 
abscess. The last three dogs were allowed to depart at the end 
of four weeks with slight pus infection. 

Since these researches were concluded, another series of ex- 
periments was undertaken upon the lines conducted by Dr. 
Carpenter, extending over a period of twelve years. These ex- 
periments were performed upon dogs, guinea pigs, rabbits, white 
mice, and humans. One hundred and seventy-six experiments 
were made. They consisted of the application of pus from 
pyorrhoea patients direct to healthy and diseased gums with a 
view of producing interstitial gingivitis or pyorrhoea alveolaris 
or both. Applications were made to fifty-six humans, twenty-six 
had slightly inflamed gums and thirty comparatively healthy 
gums. Forty-eight dogs were treated in like manner; twenty- 
nine young dogs had healthy gums and nineteen older dogs 
slightly diseased gums ; thirty-two guinea pigs ; eighteen rabbits 
and twenty-two white mice. While a slight inflammation was 
produced in a part of those cases where inflammation already 
existed, no extended chronic inflammation resulted. We would 
naturally expect to obtain some results in the white mice since 
they are of the degenerate type and very susceptible to disease 
but the results were similar to those of other animals. These 
experiments may later seem crude and with improved methods 
better results may be obtained. 

Outside of a few specific diseases of the gums and alveolar 
process some of which have already been enumerated, no one 
has demonstrated that specific pathogenic bacterial infection 
is a cause of interstitial gingivitis although the mouth is known 


to be the breeding ground of an extensive variety of germs. 
Teeth are extracted, irregular teeth are corrected, healthy gums 
are injured in filling teeth and finishing fillings many times each 
day but we seldom see local infection of the gums and alveolar 
process, producing interstitial gingivitis which comes to us every 
day for treatment. 

In these diseased conditions, mechanical specialists spend 
hours on the surgical treatment of the gums, peridental mem- 
brane and alveolar process surrounding the tooth without first 
destroying the pus germs about the teeth, injuring the parts 
and carrying the pathogenic bacteria into the wounds. If infec- 
tion were a cause, such rash treatment surely would intensify the 
disease. Some of the lower vertebrates, such as the carnivora 
live upon putrid food containing all forms of pathogenic bac- 
teria but gum infection rarely, if ever, takes place. 

Within the past year a machine has been placed upon the 
market for the supposed purpose of forcing oxygen through the 
tissues in the treatment of this disease. I have watched this 
process of treatment "with fear and trembling" since the 
method of application forces the pus germs through the inflamed 
alveolar process. Why infection does not occur is a mystery. 
This method of applying drugs and forcing pus germs into the 
tissues without infection is a strong point in favor of the non- 
infectious theory of interstitial gingivitis. 

From our knowledge based upon original researches at the 
present time, interstitial gingivitis, from the viewpoint of the 
specialist, cannot be classed as an infectious disease. It may be 
possible in the future with more improved methods of research 
to throw a clearer light on the nature of the process. 



Interstitial gingivitis is an inflammation which may take 
place in the gums, peridental membrane and alveolar process at 
any point from the gingival border to the apex of the root or 
roots of the tooth. This inflammation may be confined to a very 
small area at any one of these localities and progress to abscess 
and be restored to health without other parts becoming involved 
or the entire structure may become diseased resulting in the 
exfoliation of the tooth. 

To illustrate, among the local causes tartar or other irritants 
at the gum margin will set up a gingivitis. Remove the irritant 
and by local treatment the gums are restored to health. The 
interstitial structures have not been involved. In autointoxica- 
tion, poisons circulating in the blood may and do collect in the 
arteries midway between the gum margin and the apical end of 
the root, set up inflammation and a peridental abscess forms 
discharging directly upon the gum. The parts heal with very 
little or no pain to the patient. The gum margin or the apical 
end of the root or even the opposite side of the alveolar process 
is not involved. Here we have an interstitial inflammation. 
Again the pulp in a tooth dies, inflammation takes place at the 
apical end of the root and proceeds to abscess. Here again we 
have an interstitial inflammation without gingivitis. It is im- 
possible, in many patients, to state just when the inflammation 
begins and in most patients it is both gingival as well as deep- 
seated. The term "interstitial gingivitis" is used to cover all 
the inflammation of the gums, peridental membrane and alveolar 

Before discussing interstitial gingivitis we must first famil- 
iarize ourselves with the nature of the structures involved since 
there are no other structures in the human body like them by 
which the pathology can be compared. The structures and their 
functions are unique in themselves. We must, therefore, re- 



capitulate briefly the main points already brought out in pre- 
vious chapters in regard to the structures involved. 

In the evolution of the face, jaws and teeth the tendency is 
for these structures to grow smaller, hence the jaws and alveolar 
process are transitory organs. In this natural evolution the 
influences of the parents, owing to excesses tend to produce tired 
out reproductive organs; these fagged out reproductive organs 
in turn tend to produce an unstable nervous system in both 
mother and child. The most intense effect is on structures 
which are transitory and always tend toward the least 

After birth, the child is subjected to one or all the children's 
diseases which also tend to produce an unstable nervous system 
in the child. The effect of an unstable nervous system upon the 
child is to produce an arrest of development of transitory struc- 
tures and acts also towards the line of least resistance. In both 
conditions, that of the parents and that of the child, the ten- 
dency is to produce a still smaller jaw and alveolar process. 

Again, .in some of the lower vertebrates, there is a succession 
of teeth throughout life. In the higher vertebrates, including 
man, there are only two sets ; one is shed as soon as it has served 
its usefulness by absorption of the alveolar process and a second 
set takes its place. As soon as the alveolar process has built 
itself about the teeth, the phylogenetic influence is ready to 
remove the second teeth. In other words, the alveolar process 
is only waiting for some irritant to set up a low form of inflam- 
mation to produce absorption of the bone. "We, therefore, have 
in the alveolar process a doubly transitory structure. We have 
also in the alveolar process an exceedingly sensitive end organ. 
The tooth to all intents and purposes, so far as this disease is 
concerned, is a foreign body. The arteries and nerves pass 
through the bone in a tortuous manner as far as the root of the 
tooth. Poisons circulating in the blood pass to the end of the 
arteries and stop setting up irritation and inflammation. 

There are other end organs in the body but they are all com- 
posed of soft tissues. These tissues can and do expand when in- 
flammation is set up and in many instances recover health. Not 
so with the alveolar process. When inflammation takes place in 


this tissue, expansion of the arteries cannot take place and de- 
struction occurs. The process rarely if ever recovers its lost 
tissue. Because the alveolar process is a transitory structure 
and end organ, it is the first structure in the body to respond to 
poisons and toxins. Two illustrations are only necessary to 
prove this statement. When a patient who has been working in 
metals or drugs visits his physician for any ailment, the first 
thing the physician does is to examine the gums to ascertain if 
the patient is poisoned by the drugs or metals, this structure 
being the first to become diseased and register the poisons. 

Again, when the physician administers mercury or potassium 
iodid in the treatment of a specific disease, he continues the 
treatment until the gums are "touched" (inflamed), this symp- 
tom being the first and only sign that the system is under the 
influence of the drug. In lead poisoning we have the blue gum ; 
in mercury, red ; brass, green ; scurvy, red, etc. The colors are 
due to the kinds of poisons collected in the ends of the capillaries 
next to the root of the tooth. These indications are sufficient 
proof of the statement that the alveolar process is the first 
structure involved. 


It is not my intention to enter into a minute description of 
the phenomenon of inflammation but to simply state as briefly 
as possible how it is produced and the changes which take place 
in the tissues involved in the disease under discussion. 

The most simple illustration of active inflammation in a 
highly vascular tissue is that of an injury to the fairly trans- 
parent web of the hind foot, tongue or mesentery of the frog. 
The web of the foot of a small frog is so thin that the changes 
occurring in and around the vessels of the part injured can be 
readily found with the microscope. 

With slight modifications due to local conditions in the tis- 
sues under examination, the process of inflammation is the 
same throughout the entire vertebrate series from the reptilia 

The frog is prepared by destroying the central nervous sys- 
tem or spinal cord by passing a wire through the vertebral col- 



umn after first being- curarised. The web of the foot is then 
placed under the microscope and a wound is made with a needle. 
The first change noticed in the surrounding tissue of the injured 
membrane is a dilatation of the vessels first of the arteries and 
then of the veins. In the arteries, there is a very noticeable 
acceleration of the flow of blood. At this early period, there is 
very little evidence of dilatation of the capillaries. In the course 
of an hour, however, expansion can be readily observed and the 
former invisible capillaries now fill with blood and are quite 
easily observed. In the course of an hour or two there is a slow- 
ing of the blood current. Before the wound was made, there was 
a well-marked central stream of corpuscles with an outer zone of 
plasma devoid of corpuscles. Now the central stream of cor- 
puscles broadens out and the center zone of plasma becomes 
smaller and smaller. As it narrows, there is an increasing num- 
ber of clear round blood leucocytes observed traveling at a 
slower rate than the central stream and occasionally stopping 
beside the walls of the vessels and after a short detention con- 
tinue their course. The leucocytes act as though they wish to 
attach themselves to the walls of the vessels. The current be- 
comes slower and slower until there is a vast distinction between 
the central and the peripheral streams. The corpuscles are now 
closely packed together and fill the whole surface of the blood 
vessel. The leucocytes now approach the vessel walls in large 
quantities and adhere more firmly. While the current is 
recognizable the action of the stream causes the leucocytes to 
assume a pear-shaped appearance the larger round end pointing 
in the direction of the current. As the blood stream gradually 
slows the corpuscles may at last move in a series of movements 
with the beats of the heart, while frequently in the veins and cap- 
illaries the mass of blood may be seen moving in one direction 
or the other. Frequently one or the other of these stages is 
followed by complete stasis of blood in the vessels of the injured 
area for occasionally little or no arrest is seen in the vessels. 
Accompanying this stage, there is already considerable exuda- 
tion of clear fluid from the wound; there is an out-pouring of 
lymph from the distended vessels. With the slowing of the 
stream the leucocytes collect next to the walls of the small veins 



and within the capillaries and pass from the interior to the ex- 
terior of the vessels. (Fig. 29.) These leucocytes after passing 
through the walls of the vessels collect in the lymph spaces be- 
tween the vessel walls. There may also be found a small number 
of red corpuscles distributed among them. The leucocytes do 
not stop near the vessels but by an active amoeboid movement 
they pass on to the point of injury. Then by the end of about six 
hours the surrounding area of the injury may be covered by a 
serum filled with leucocytes. Here then we trace the first step 
towards the provisional protection of the wound. 

Tig. 29. — Inflamed Human Mesentery (Osmic-acid Preparation) ; a, Normal 
Trabecula; b, Normal Epithelium (Endothelium); c, Small Artery; id, 
Vein with Leucocytes Arranged Peripherally; e, White Blood-Cells, 
Which Have Emigrated or are Emigrating; f, Desquamating Endothelium; 


If, in producing this wound irritating substances have not 
entered, the process may be arrested at this point. The stasis 
of blood in the distended vessels may now be followed by a 
restoration of the current and slow return of the vessels to their 
former caliber will take place. 

On the other hand, if irritants of a microbic nature enter the 
wound the process may extend to abscess. If the irritants, in- 



fections or poisons are too abundant, migration of quantities of 
leucocytes takes place and they collect between the bundles of 
connective tissue fibers. The cocci collect in the lymph spaces 
and the massing of leucocytes corresponds to the accumulation 
of the microbes. At the end of about forty-eight hours a com- 
plete abscess forms, separated sharply from the surrounding 
healthy tissue. In the center all traces of previous blood vessels 
are lost, while in the periphery they are easily traceable ; in the 
center of the abscess the original tissue has wholly disappeared, 
while near the outer surface, sheaths and bundles of disinte- 
grating fibers are seen; about the tenth day new growth of tis- 
sue begins to show itself. Numerous capillaries and newly- 
formed connective tissue are seen and the process of restoration 
takes place. 

We have shown, in a general way, the different stages of 
inflammation in soft tissues of all vertebrates, including the 
gums and peridental membrane in man. The inflammatory proc- 
ess which takes place in the alveolar process, however, is quite 
different in its procedure. Instead of the traumatic injury to 
the frog just cited, the injury to the alveolar process is brought 
about by the poisons and toxins circulating in the blood and 
which I have called constitutional causes. These poisons and 
toxins take the form of local disturbance, of innervation, poor 
circulation and tissue metabolism. Generally the action of 
poisons is to contaminate all the blood which circulates to the 
remote organs. This general action of the poisons and toxins in 
the blood is added to the local action of irritants. These poisons 
act upon the nerve sheaths, decompose the blood but mainly 
affect the vessel walls. They also tend to accumulate in certain 
organs within which they frequently develop their chief action 
and often cause remarkable tissue change. 

The principal structures affected by these poisons are the 
end organs, namely, the eye, the brain, the kidney recognized by 
every physician, while the dental pulp and alveolar process, 
which I have previously mentioned, are the most complete end 
organs in the human body and usually first involved. Because 
of the nature of their structures and surroundings, symptoms of 
disease are observed in these structures long before the other 
end organs are affected. 



The dental pulp (as before stated) is the most complete end 
organ for the reason that the blood enters the tooth by a single 
artery. It then multiplies until the pulp is composed of myriads 
of minute arteries confined within bony walls. The return blood 
again passes through the apical end of the tooth by a single 
vein. It is not uncommon, therefore, for the arteries, filled with 
poisons, to expand and prevent the return to circulation, thus 
causing numerous diseases and frequently spontaneous death of 
the pulp. 

The second most complete end organ is the alveolar process. 
It is the only bony end organ in the human bod}-. The arteries 

Fig. 30. — Is Similar to Fig. 10. The Haversian Canal Shows a Dark Line 
Around the Inner Border Representing the Arterial Wall. — The Space 
Between the Dark Line and the Bone is Filled with Fibrous Tissue. 

penetrate the bone in a wavy manner as far as the root of the 
tooth, which, so far as the disease is concerned, is a foreign body, 
when circulation ceases to any great extent. 

The simplest illustration of the action of these poisons is 
that of a healthy individual at the sixth period of stress or 
about sixty years of age. This senile period, however, may take 
place at a much earlier time in life. The excretory organs be- 
come weakened and the poisons formerly excreted by the lungs, 
kidneys, bowels and skin are not eliminated but circulate in the 
blood. Odor from the breath, skin fscces, an abnormal urinary 


acidity degree, indican and oilier poisons in the urine indicate 
these changes. These poisons arc retained in the peripheral 
organs but more especially in the dental pulp and alveolar proc- 
ess. Those receiving the greatesl quantity and retaining it are 
the ones so constructed as to prevenl a return of the irritants or 
poisons to the circulation. 

The irritants cause a dilatation of the vessels, first of the 
arteries and then of the veins. This dilatation of the arteries 
presses againsl the bony walls of the alveolar process which 
sets np absorption. ( Fig. .'!<>.) Since the poison is a general one 

Fig. 31. — Bone Absorption e» Halisteresis : In the Middle Space the Bone is 
Just Beginning to Absorb Ground the Artery. The Space to the Left 
Shows a Large Portion oe Bone Absorbed, Leaving ink Fibrous Tissue in 
Place; While the Two Spaces at the Right and Bottom op the Illustration 
Show the Lime Salts ami Fibrous Tissue Entirely Destroyed. 

many arteries act in like manner. Chemical changes also take 
place around the arteries which assist greatly in producing bone 
absorption. Balisteresis is produced and the hone quickly dis- 
appears. Sometimes, especially when only a small area is in- 
volved lacunar absorption only occurs. The vessels of Von 
Ebner (capillaries) being much smaller, the irritation is not so 
intense nor is the effect of pressure or chemical changes upon 
the surrounding hone so great. The area of absorption, there- 



fore, is limited, resulting in small canals from one Haversian 
canal to another or from one absorbed area by halisteresis to 
another. The tissue around the artery now is not unlike the 
soft tissue previously under consideration and the natural proc- 
esses of inflammation continue. In many patients the process of 
inflammation stops with the absorption of bone. The tooth or 
teeth now are simply attached to normal fibrous tissue. In many, 
the inflammatory process proceeds a little further. There is 
now acceleration of the blood stream which later slows consid- 
erably. The central stream of corpuscles broadens and the outer 
zone of plasma grows smaller and smaller. The same process 
takes place in reference to leucocytes, red blood corpuscles and 
exudate as before (Fig. 31) and if there is sufficient irritation 
and infection, an abscess will form in the matrix or fibrous tissue 
which originally contained bony tissue. It will be seen, there- 
fore, that the rigid bony framework of tissue prevents great 
vascular dilatation without bone absorption. It may, however, 
be the seat of great pain, due to pressure of the confined exudate 
upon nerve endings. 

Local changes in function such as want of proper articula- 
tion ; too great pressure in mastication on one or more teeth ; 
slight change in position of teeth after they have once become 
solid in the jaw; destroying pulps and filling roots so that the 
peridental membrane is required to do more work ; hypertrophies 
of roots; teeth that have once been abscessed and were appar- 
ently restored to health, etc., are a few of the local causes which 
earlier set up inflammation in the alveolar process by the irri- 
tants and poisons in the blood stream than in the normal adjoin- 
ing teeth. 

Local irritations such as wedging of teeth for filling ; correct- 
ing irregularities of the teeth, etc., which have already set up 
local inflammation are fruitful sources and weak localities for 
the irritations in the blood stream to quickly renew inflamma- 
tion and destruction of the alveolar process. 

One of the best illustrations of the effect of poisons in the 
blood acting upon weak abnormal structures in the jaw is that 
of phosphorus poisoning. It is known that persons working in 
phosphorus, such as match-making, are liable to phosphor ne- 


crosis of the jaws. When it occurs, it is usually associated with 
a carious or diseased tooth. It is supposed that the phosphorus 
enters the jaw through or around the tooth. This, however, is 
not the case. The poisons circulating in the air are taken into 
the system through the lungs or if handled by the hands through 
the skin. It thus enters the blood and causes a general disturb- 
ance of nutrition. The blood vessels become charged with the 
poison and the taking in of oxygen is considerably diminished. 
In consequence, degeneration of tissues results. The red blood 
corpuscles change their color and break down. The nervous sys- 
tem, especially the peripheral nerves degenerate. The arteries 
in the alveolar process are the first to become diseased. The 
parts of the jaw which first feel the effect of the poison are those 
parts where the teeth have lost their normal function, more 
particularly teeth with dead pulps whose roots may or may not 
be filled, with or without slight inflammation, teeth which have 
abscessed or been wedged or are doing more work than normal. 

When absorption has taken place, the bone is not restored 
after the person has obtained his growth, the transitory nature 
of the process and only two sets of teeth being natural to man. 
If the process be removed from any cause (even if the perma- 
nent teeth be still in the jaw) it is not restored. 

The absorption of the alveolar process, under constitutional 
causes, usually begins at the gingival border because of its thin- 
ness of structure. The gum tissue does not change but follows 
the bone, in its absorption, until the tooth is exfoliated or until, 
under treatment, the alveolar process is restored to health, when 
the gum attaches itself firmly to the bone and is restored to its 
normal condition. 

We have shown the simple process of inflammation to the for- 
mation of abscess and the absorption of bone in relation thereto 
in the milder forms due to traumatism, toxins and poisons, but 
the procedure under severe constitutional conditions is much 
more intense. 

The transitory nature of the alveolar process, its sensitive- 
ness as an end organ, when inflammation is once set up in the 
gums, alveolar process or peridental membrane, due to either 
local or constitutional causes, compels it to become chronic with 



disastrous results which are difficult of treatment and of restora- 
tion to health, especially if the vitality of the patient is low. 
This inflammatory process is along the line of least resistance. 


There is much discussion by certain writers in regard to the 
action the nervous system plays in inflammation. Some take 
the stand that the central nervous system does act upon the 
blood vessels in a given locality while others claim that it must 
be a peripheral nervous mechanism which controls the blood ves- 
sels. Experiments have shown that the vascular changes con- 
nected with inflammation can occur independently of the central 
nervous system. It follows then that there may be a peripheral 
nervous mechanism controlling the vessels. 

It has been demonstrated by Klebs x that the endothelial walls 
of the capillaries do contract. The conclusion then is that the 
endothelium of the capillaries is, to some extent, self regulating. 
It is quite possible that the muscular coats of the smaller ar- 
teries and capillaries act to stimuli. 

Thoma - says, "It is evident, however, that the local circula- 
tory reaction after injury depends upon the condition of the 
cerebro-spinal vasomotor centers and that the peripheral vaso- 
motor nerve apparatus may also act independently. From what 
has been said it appears that among the direct action of trau- 
matism, injury to the nerves is of great importance. This injury 
to the nerves at the site of the lesion is either a change in the 
invisible molecular structure of the nerve fibers, or one which 
can be recognized under the microscope. Each change in the 
molecular structure of the nerve causes a change in its excitabil- 
ity which is termed 'nerve irritation' by physiologists. This irri- 
tation is frequently more or less painful, and is perceived sub- 
jectively as pain. The disturbance of the innervation of the 
vessel wall, however, is to be clearly distinguished from the sen- 
sation of pain. The former also is partly caused by the direct 
action of the injury to the vasomotor nerv apparatus contained 

1 Klebs. Allg. Pathologie. 

2 Thoma. Pathology and Pathological Anatomy. 


in the injured area. The disturbance of vasomotor innervation, 
however, is seldom strictly limited to the area directly affected 
by the injury, since the nerve irritation both directly and re- 
fiexly alters the excitability of the vasomotor centers in the walls 
of the neighboring arteries, and thus causes the local circulatory 
reaction. ' ' 

My researches have shown that the nerve supply in the alveo- 
lar process, as compared with that in the peridental membrane 
and periosteum is very slight. Inflammation and infection, 
therefore, taking place in the peridental membrane at the apical 
end of the tooth root forming alveolar abscess or at the side 
nearest to the apical end where peridental abscess forms, where 
the alveolar wall is quite thick, pain is much more severe than 
when the abscess forms in or near the gingival margin of the 
process. On account of local and constitutional irritations, 
nerve end degeneration in alveolar absorption is the rule. Pain, 
however, in this instance is not as severe in abscess formation in 
the alveolar process as in other bones. 

These local and constitutional irritations produce paralysis 
and finally death of the nerve fiber. When degeneration or death 
of the nerve fiber takes place, the action upon the coats of the 
arteries is such that inflammation and absorption of the alveolar 
process ensues. 

The local irritations and infections produce the same effect 
upon tissue in inflammation as the internal (constitutional) irri- 
tations and infections. Adami 3 says, "Anything which causes 
local injury to the tissue is a cause of inflammation, be it a me- 
chanical trauma, a physical insult, as by heat, cold or electricity, 
a disturbance brought about by altered metabolism and abnor- 
mal internal secretions, or bacterial or microbic invasion and 
growth. This last is the commonest cause of acute reaction and 
differs from the physical and mechanical causes (although not 
from metabolic disturbances) in that, as a cause, it is not of 
momentary duration, but of continued. It is not the mere physi- 
cal entry of microbes into the tissues that induces inflammation 
but the liberation of them of their products in growth or disin- 
tegration. And so long as those products are being liberated, 

* Adami. Principles of Pathology, Vol. 1, page 420. 


for so long* is the cause of action. It differs from the metabolic 
causes in that the latter induce tissue irritation of a milder grade 
and do not induce acute, but rather chronic reaction." 

Kirk 4 says, "Viewed as an inflammatory process we have, 
then, in the study of pyorrhoea (interstitial gingivitis) to regard 
its clinical or objective phenomena as reactions of the retentive 
tissues of the teeth toward injuries inflicted by mechanical 
trauma, physical irritants, altered metabolism, the toxic effects 
of altered secretions, or by the t oxic p roducts^ of microbic or 
•7 bacterial invasion. Any of these agencies, severally or collec- 
•- tively, may induce such changes in the retentive structures as 
will lead to their molecular necrosis and the ultimate exfoliation 
of the teeth, the process constituting comprehensively what we 
know as pyorrhoea alveolaris (interstitial gingivitis)." 

The process of inflammation from local irritation and infec- 
tion proceeds in the same manner as the traumatism upon the 
web of the frog's foot. 

Patients who have been ill for any length of time, such as 
those suffering with phthisis, lues, kidney lesions or other linger- 
ing diseases, and those with low vitality, take on interstitial gin- 
givitis much more readily than those of strong vitality. 

Summing up this chapter, no matter whether the irritation 
be local or constitutional or both, the inflammation set up thereby 
is progressive in its nature and does not cease until the tooth 
or teeth have been exfoliated by the absorption of the alveolar 
process, although treatment, changes in environment and sys- 
temic conditions may check the disease for a limited time. The, 
inflammation is solely the cause of bone absorption and may be 
slow or rapid in its action. r 

American Text-Book of Operative Dentistry, Fourth Edition, page 470. 



All vertebrates possessing two sets of teeth during life 
the roots of which are situated in bony sockets have interstitial 
gingivitis to a greater or lesser extent. The mere fact of 
the eruption and shedding of the teeth, as in human, is an 
indication that there is an inflammatory process present. Wild 
animals leading a natural, normal life are less liable to have 
this disease than those having become domesticated. Wild 
animals domesticated and tamed animals taken out of their 
natural environment suffer with this disease to as marked a 
degrees as human. While it is true animals, as a rule, do not 
suffer with the nervous types of disease like human, yet a wild 
animal in confinement with artificial feeding must suffer, to 
a greater or lesser extent, according to the nature of the change 
and the amount of restlessness produced. Changes in vital 
resistance are not as frequent or as marked in animals as in 
human, yet wild as well as domesticated animals do occasion- 
ally suffer with disease and changes in vital resistance. 

Wild animals roaming at large and obtaining their food 
are in a much more natural environment than when in captiv- 
ity. The organs of the body are performing their natural 
functions, and thus elimination is carried on normally. Old 
age, even in animals living in their natural wild environment, 
predisposes weakened eliminating organs, while these, in turn, 
owing to poisons in the blood, will cause interstitial gingivitis 
and finally loss of teeth. 

Wild animals under domestication owing to change of envi- 
ronment can best be studied in relation to this disease. A visit 
to the great Zoological Gardens in Dublin, London, Hamburg, 
Paris, New York City or Chicago, and a careful study of the 
mouths and jaws of the animals there confined will readily 
convince the investigator of the truth of these statements. 
Monkeys are probably more susceptible to disease and death 



than most animals. Cows fed upon brewers' slop and con- 
fined indoors have interstitial gingivitis badly; horses which 
have been biting grass with their front teeth, living in the sun- 
shine and breathing the fresh air, when returned to the stable in 
the Fall begin to "crib," biting the woodwork around the 
stall. The front teeth feel uncomfortable because of the entire 
change of environment. The "cribbing" causes the blood to 
be forced out of the capillaries of the peridental membrane, 
and for the time being gives relief to the animal. It soon 
returns and because of the pain the process is repeated. In 
the course of a week or two, however, the eliminating organs 
adjust themselves to the new environment and the teeth remain 
comfortable. House animals are very prone to interstitial 
gingivitis as well as to other constitutional diseases. In most 
animals of this kind they are taken out of their natural envi- 
ronment, and autointoxication and disease is the rule. The 
carnivora suffer with pyorrhoea alveolaris to a more marked 
extent than the herbivora owing to the fact that they subsist 
to a great degree upon pus-ladened nitrogenous food, thus 
infecting the gums and peridental membrane. Dogs with this 
disease are the best animals for research. 

As the first step in investigation, two practitioners of 
comparative medicine, with an extensive hospital practice 
(Dr. Charles E. Sayre and Dr. Alsop E. Flower), were con- 
sulted as to the frequency of this disease in animals. All 
animals under their care suffered from it more or less, but 
eighty per cent of dogs over eight years of age had the dis- 
ease. Nearly every dog in the hospital under their care was 
so affected. These dogs comprised all breeds, from spaniels 
and terriers to the Newfoundland, St. Bernard and great Dane. 
On examination, every phase of interstitial gingivitis was found 
in the mouths of these dogs, from its inception to the loss of 
the teeth. The number of dogs observed was twenty-seven. 
The roots of the teeth of some were covered with deposits 
and so exposed that the teeth could be removed with the fin- 
gers. Such diseased mouths are rarely, if ever, present in 
human beings. The outer plate of bone was absorbed, the roots 
entirely exposed, pus was oozing from around them and the 
mucous membrane was badly inflamed. 


It = - 


- - - 

staJ - ... - 



stitutional defects than in man. Some were old and blind. 
Some had been injured and were under treatment for wounds. 
Some were suffering from rachitis, nervous diseases, and were 
overbred. Others were constipated or had germ types of diar- 
rhoea. One had kidney inflammation and bronchitis with high 

Fig. 33. — The Mouth of a Boston Terrier; Owing to Illness Interstitial Gingi- 
vitis has Caused Absorption of Bone and the Incisors and Molar were 
Removed by the Fingers. 

fever. In short, these dogs, being house dogs, presented most 
of the constitutional diseases to which man is liable. 

The mouth of a Scotch terrier is shown in Fig. 32. The 
molar and premolar had been removed with the fingers. The 
cuspids and incisors are quite loose. There are large deposits 



of tartar. The gum and alveolar process have been absorbed 
nearly one-half the length of the roots of the teeth. In Fig. 33 
is seen the mouth of a Boston terrier with the incisors and 
premolars removed. There is extensive pyorrhoea. There are 
calcic deposits upon the cuspids and molars. There is recession 
of the gums and alveolar process. In Fig. 34 is shown the mouth 

Fig. 34. — The Mouth of Another Boston Terrier; One Tooth has been Re- 
moved and Interstitial Gingivitis is Seen Around the Other Teeth. 

of another Boston terrier. In it one premolar in the upper and 
one on the lower jaw have been extracted. There is extensive 
inflammation of the gum about the molar, cuspid and incisor 
with large calcic deposits about the teeth. In Fig. 35 are shown 
teeth covered with calcic deposit the entire length of the root. 


These teeth were removed by the fingers from the mouths of two 
dogs, one of which was later obtained for scientific study. This 
was all the material to be obtained from the hospital, since the 
dogs were pets which had been placed under treatment by their 

Through the courtesy of Poundmaster Hugh Curran, the 
necessary material was obtained from the Chicago Dog Pound. 
Here from four hundred to a thousand dogs are killed per week 
during June, July and August each year. Ninety-five per cent 
are mongrel curs leading a street life, hence neither luxurious 
diet nor luxurious care can be charged with any disease in 
them. They have, at least, plenty of outdoor exercise and fresh 
air. Many, despite this reversion to the life of their wolflike 
ancestors, have skin diseases and are deaf and blind from old 
age. The bodies were secured after death, at which time exam- 


Fig. 35. — Snows Teeth of a Dog Covered with Calcic Deposits which were Quite 
Loose and were Removed by the Fingers. 

inations of the mouths were made. Five per cent of the dogs 
entering the pound are of good breeds. These, if not called for 
by the owners, are sold for a moderate price. 

The dogs selected for the death penalty are collected in a 
large box pen, leading out of which is a door through which they 
pass into an air-tight box. Communicating with this box is a 
stove in which sulphur is burned with charcoal. The fumes 
pass into the box and death is almost instantaneous and painless. 
After they remain fifteen minutes, a door leading to the air is 
opened and the bodies are carted away. It was at this time that 
access was had to them. The mouths were then examined. Such 
cases as were of interest were placed on one side and the jaws 
removed from the bodies. Inside of one-half hour the specimens 
were in a solution to be kept until desired for use. Jaws (with 
interstitial gingivitis in all stages of progress, from simple in- 


flammation of the gums to the most extreme cases of exfoliation 
of the tooth) wore obtained in an abundance for future studies. 
It is not an easy matter to ascertain the ages of these animals. 
In a general way, it was found that inflammation of the gums, 
especially about the canine teeth, was almost always present in 
dogs over one year. About twenty-five per cent of these dogs at 
lour years of age had the disease, eighty per cent at from eight 
to ten years, ninety-five per cent over twelve years of age. 
Since I commenced my investigation (twenty years ago), I have 
examined quite a Large number of dogs about homes, but have 
never found a dog over four years without this disease to a 
greater or less extent. Many house dogs at one year had inflam- 
mation of the gums. Dogs for infection and those used for mer- 
curialization were picked up in the streets. 

Most of the dogs exhibited at dog shows are young, ranging 
from one to four years of age. About twenty-five per cent would 
range four years to eight. A casual examination of their mouths 
revealed interstitial gingivitis. Occasionally recession of the 
gums and pyorrhoea alveolaris occurred. On a more careful ex- 
amination, twenty-five per cent of dogs between the ages of one 
and four were found to have interstitial gingivitis and seventy- 
five per cent of dogs from four to eight years were found to 
have interstitial gingivitis with recession of the gums and pyor- 
rhoea alveolaris. In the study of this disease, therefore, dogs 
are excellent substitutes, since for pathologic research they can 
be obtained at any stage of the disease. 

The technique of the examinations of interstitial gingivitis 
and pyorrhoea alveolaris in dogs was as follows: After fixing 
and hardening in two per cent formalin, alcohol, or Midler's 
fluid, the tissues were decalcified in a five per cent alcoholic solu- 
tion of nitric acid, imbedded in celluloidin and stained in various 
ways, the principal ones being hematoxylin and eosin. Ten or 
more slides would be obtained from each tooth. Out of these 
slides have been selected a series illustrating the progress of the 
disease from beginning to the loosening of the tooth. 

Fig. 3b' is a longitudinal section of a cuspid tooth with the 
alveolar process in situ. A illustrates the enamel of the tooth, 
(E) the epithelium passes from the outer margin to the lower 



X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-tuird. 

Fig. 36. — Longitudinal Section of Tooth and Gum Tissue. Slight Gingivitis. Dog. 

A, Enamel. E, Epithelial Tissue. G, Submucous Membrane. M, Fibrous Tissue. 
SI, Slight Inflammation. 

'5. A. A. obj. 

Micro-photograph, reduced one-third. 

Fig. 37. — Longitudinal Section of Tooth and Gum Tissue. Chronic Interstitial 
Gingivitis. Dog. 

A. Enamel. E, Epithelial Tissue. G, Submucous Membrane. H, Periosteum. 
K. Capillaries. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue 
and Peridental .Membrane. RR, Space Pocket from want of Union of Epithelial Fold. 

X "■"). A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 38. — Longitudinal Section of Alveolar Process and Peridental Membrane. 
Slight Interstitial Gingivitis, Extending into Alveolar Process. Dog. 

J, Alveolar Proce 

L\ Inflammation Extending through Enlarged Haversian Canals. 
I 1 , Inflamed Peridental Membrane. 

X 75. A. A. obj. Zriss. Micro-photograph, reduced one third. 

Pig. ."•'.». Longitudinal Section of Alveolae Process &.nd Peridental Membrane. 
Chronic i [terstitial Gingivitis, Extending into Alveolar Process. Dog. 

II, Periosteum. .1, Alveolar Process. V, Violenl [nflammation. A.\, Poinl of 
Union of Epithelial Tissue and Peridental Membrane, r, [nflamed Peridental Mem 
brane. I.', [nflammation Extending through Enlarged Eaversian Canals. 


border, then folds upon itself and extends down the side of the 
crown of the tooth as far as the neck. Unfortunately, in this 
specimen, the structure connecting the epithelium and the fibrous 
tissue of the periosteum has been destroyed. The papillary layer 
of the sub-epithelial tissue is plainly shown at the outer border. 
Small round-cell inflammation may be seen extending along the 
border of this layer. It can also be observed extending down 
the capillary blood vessels into the submucous tissue (SI and G). 

Fig. 37 shows a similar section of another tooth. Here the 
epithelial structure (E) is pulled away slightly from the edge of 
enamel (A). In this section the infolding of the epithelium is 
shown at the neck of the tooth. This structure passes downward, 
folds outward and upon itself (AA) and returns two-thirds of 
the distance toward the gingival border, leaving a pocket (RR). 
The epithelium (E) is very dense and thick. The papillary 
layer of the submucous tissue (G) is very clearly defined. The 
capillaries (K) can be distinctly traced from the deeper fibrous 
tissue through the submucous layer into the papillary layer. 
The thick and heavy fibrous tissue of the periosteum ("Dental 
Ligament," Black) may be seen at H, inserted firmly into the 
cementum and extending outward and downward. Just below 
(AA) may be seen the interlacing of the coarser fibers of the 
periosteum with the finer fibers of the submucous tissue. Chronic 
round-cell inflammation may be seen extending from the papil- 
lary layer through the capillaries into the interstitial tissue of 
the submucous layer and the periosteum. Marked inflammation 
has occurred at V. The openings in the folds of the epithelium 
are fruitful sources for the accumulation of food, epithelial 
scales and detritus, in which fermentation and decomposition 
from micro-organisms result, producing inflammation. 

Pig. 38 is a section through the peridental membrane (I) and 
alveolar process (J) at the lateral incisor. The inflammation 
has extended down from the papillary layer through the sub- 
mucous tissue, the fibrous tissue of the periosteum into the peri- 
dental membrane and into the alveolar process. Round-cell in- 
flammation may be seen in the blood vessels extending through 
the Haversian canals (L 1 ). 

Fig. 39 is a similar section from another tooth showing 


chronic inflammation extending throughout the peridental mem- 
brane (I) and alveolar process (J). The Haversian canals (L) 
are well outlined by the inflammatory progress. Marked inflam- 
mation has resulted at V and also at the margin of the alveolar 

Fig. 40 is a section of the peridental membrane and alveolar 
process, illustrating the effect of interstitial inflammation upon 
the blood vessels and alveolar process. Chronic inflammation 
extends throughout the peridental membrane with very decided 
inflammatory change (V). The cut ends of the blood vessels 
which were originally situated in the Haversian canals are seen 
(BV). They have become involved with the result of a thicken- 
ing of the walls and endarteritis obliterans. The bone about 
these vessels has been entirely absorbed. The inflammation 
has extended beyond, into and through the Haversian canals, 
producing the type of absorption of the trabecular known as 
halisteresis ossium. Lacunar absorption has also occurred (0). 
Where decided inflammation (V) has taken place, abscesses are 
more liable to occur (as will be noticed later) from the large 
number of blood vessels at this locality. 

Fig. 41 is a section from another location of the alveolar 
process with a greater amplification, showing the inflammatory 
process extending through the alveolar process. Endarteritis 
obliterans may be seen in different localities (EO). Three forms 
of absorption are evident in this figure : Enlarged areas arising 
from absorption of the trabecular (halisteresis ossium) due to the 
inflammatory process. The vessels of Von Ebner precede per- 
forating canal absorption (BB), distributed over the entire field, 
also the result of the inflammatory process and lacunar absorp- 
tion (O) which may result from inflammation. As long as the 
fibrous tissue remains in these large areas to retain the osteo- 
blasts, new bone tissue may be produced under favorable condi- 
tions. On the other hand, when this tissue and the osteoblasts 
are destroyed, the alveolar process cannot be restored. 

Fig. 42 shows a section of the alveolar process from another 
dog. Here lacunar and other absorption (halisteresis ossium) 
are well shown. Thirty-seven osteoclasts (0) may be counted in 
the field while destruction of bone by halisteresis (Q) is rapidly 


going on. Remains of Haversian canals with the blood vessels 
may be seen (BV, L). In the discussion of the peridental mem- 
brane extending into the alveolar process (page 37), particular 
attention was called to the fact that large bundles of fibers ex- 
tended into the process in such a manner as almost to isolate 
portions of bone. In the lower left-hand corner (X) may be 
seen two pieces of the alveolar process entirely separated from 
each other and the main body of the bone. In interstitial gingi- 
vitis, it is not uncommon to find pieces of the alveolar process 
separated by halisteresis and lacunar absorption. When loose 
teeth are extracted as a result of this disease, pieces of the alveo- 
lar process come away with the peridental membrane attached to 
the tooth. Fig. 89 was obtained in this manner. In the upper 
left-hand corner may be seen eight or ten new osteoclasts (0) 
in an enlarged Haversian canal, at work isolating one piece of 
the alveolar process from the other. 

Fig. 43 shows a slide from still another dog. Halisteresis 
(Q) and perforating canal (P) absorption are here well shown. 
In the larger space at the lower left-hand corner may be seen 
two arteries (EO) which were originally the location of Haver- 
sian canals and which have thickened walls and a tendency to 
obliteration. The light color shows decalcification, the dark nor- 
mal bone. At P may be seen perforating canal absorption. At 
FGr fat globules may be seen, while in the larger space at the 
upper right-hand corner is evident entire destruction of the 
fibrous tissue. 

Fig. 44 illustrates a cross section of alveolar process and 
cuspid root, showing absorption of the root. Inflammation 
extends throughout the peridental membrane (I). The capil- 
laries (K) are quite numerous. These are cut both crosswise 
and lengthwise. Absorption (S) of the root may be seen pro- 
gressing at these localities. 

Fig. 45 shows a longitudinal section of the end of the root. 
Active destruction has been going on both in the pulp chamber 
(D) and at the external surface of the cementum (C). The irri- 
tation and inflammation has caused the odontoblasts to fill up 
the pulp chamber with secondary dentine, and obliteration of the 
chamber has taken placn. Below the constricted pulp may be 

Li . 


— J. 



X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 4(i. — Longitudinal Section of Tooth, Alveolar Process and Peridental Mem- 
brane. Violent Round-Cell Inflammation of Peridental Membrane, Ex- 
tending through the Haversian Canals into the Alveolar Process. 

C, Cementum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. N, Large 
Spaces arising from Absorption of the Trabecular, starting in the Haversian Cabals 
(Halistcresis). O, Lacunar Absorption. V, Violent Inflammation. BV, Blood 
Vessels, originally Haversian Canals. P, Inflamed Peridental Membrane. L 1 , Inflam- 
mation Extending through Enlarged Haversian Canals. 

X 150. D. D. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 41. — Longitudinal Section of Alveolar Process. Chronic Inflammation Ex- 

Absorption. Dog. 

J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecular, 
starting in the Haversian Canals (Halisteresis). O, Lacunar Absorption. P, Perforat- 
ing Canal Absorption. BB, Blood Vessels of V. Ebner preceding Perforating Canals. 
EO, Endarteritis Obliterans. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 42. — Longitudinal Section of Alveolar Process. Chronic Inflammation Ex- 

J, Alveolar Process. L, Haversian Canals. N, Large Spaces arising from Ab- 
sorption of the Trabecular, starting in the Haversian Canals. O, Lacunar Absorption. 
Q, Halisteresis Ossium or Decalcified Bone. X, Eemains of Calcified Bone. BV, Blood 
Vessels originally Haversian Canals. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 43. — Transverse Section, Alveolar Process. Chronic Inflammation Ex- 

J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecule, 
starting in the Haversian Canals. P, Perforating Canal Absorption. Q, Halisteresis 
Ossium or Decalcified Bone. X, Remains of Calcified Bones. EO, Endarteritis Obli- 
terans. FG, Fat Globules. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 44. — Cross Section op Tooth, Alveolar Process and Peridental Membrane. 
Chronic Inflammation of Peridental Membrane and Absorption of the 
Boot of Tooth. Dog. 

B, Dentine. C, Cementum. 

D, Pulp. I 1 , Inflamed Peridental Membrane. K, Capil- 
laries. S, Root-absorption. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 45. — Longitudinal Section op the End op the Eoot op a Tooth, Alveolar 
Process and Peridental Membrane, Showing Chronic Inflammation op the 
Peridental Membrane. Exostosis op the Root op the Tooth and Lacunar 
Absorption. Dog. 

C, Cementum. D, Pulp, with 3 Foramina. J, Alveolar Process. 0, Lacunar Absorp- 
tion. P, Perforating Canal Absorption. CC, Cementosis. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 46. — Cross Section op Inflamed Peridental Membrane. Dog. 

II, Inflamed Peridental Membrane. \Y. Epithelial Debris. 

X 15. 75 M. M. obj. Spencer. Micro-photograph, reduced one-third. 

Fig. 47. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
brane, Showing Interstitial Gingivitis and Pyorrhoea Alveolaris, with 
Tooth About to be Exfoliated. Dog. 

C, Cementum. E, Epithelial Tissue. H, Periosteum. I, Peridental Membrane. 
J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, Fibrous Tissue. E, 
Pus Pockets. U, Nerve Tissue. V, Violent Inflammation. AA, Point of Union of 
Epithelial Tissue and Peridental Membrane. CC, Cementosis. DD, Calcific Deposits 
Destroyed by Acids. 

X 4(). ?,.) M\ M. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 48. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
brane and Gum Tissue, Enlarged from Fig. 42, Showing Active Inflamma- 
tion, with Pus Pocket. Dog. 

C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. I 1 , Inflamed 
Peridental Membrane. J. Alveolar Process. L 1 , Inflammation Extending through En- 
larged Haversian Canals. M 1 , Inflamed Fibrous Tissue. P., Pus Pocket. V, Violent 
Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Membrane. 

FP, Food Containing Micro-Organisms. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 49. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
brane and Gum Tissue, Enlarged from Pig. 42, Showing Active Inflamma- 
tion with Pus Pocket. Dog. 

Alveolar Process. M 1 , Inflamed Fibrous 
V, Violent Inflammation. 

C. Cementum. 

E, Epithelial Tissue. J, 
Tissue. R, Pus Pocket. 


seen three divisions of the pulp (D) extending through three 
separate canals in the cementum (C). Cementosis (CC) may 
be seen at the end of the root. Lacunar absorption is going on 
(0). Thus results a building up and tearing down of the same 
tissue from the same cause, interstitial gingivitis. 

Fig. 46 shows inflammation of the peridental membrane (I 1 ) 
with epithelial debris (W) scattered throughout the field. 

Fig. 47 is a section through the jaw and incisor tooth, show- 
ing the relation of the structures to each other in a severe case of 
interstitial gingivitis and pyorrhoea alveolaris. The tooth is at- 
tached at only a very small portion of the apical end of the root. 
The disease has been of long standing. Absorption of the alveo- 
lar process on one side has progressed on fully one-half of the 
root, while upon the other about one-third the distance. Inflam- 
mation commenced at the gingival border and extended through 
the periosteum (H), peridental membrane (I) and alveolar proc- 
ess (J). Marked inflammation (V) has occurred in the mucous 
membrane fold. An abscess has formed with a fistula extending 
to the gingival border. The thin border at the left of the fis- 
tulous tract is the epithelium layer next to the tooth. It is evi- 
dent that the pus burrowed to the surface through the struc- 
ture instead of between the epithelium and the tooth. A similar 
abscess and fistulous tract are evident upon the gingival border 
on the opposite side of the tooth. The irritation produced by 
the movement of the tooth has caused the cementoblasts to de- 
posit large quantities of material upon the sides and the end of 
the root. The main nerve trunks (U) may be seen at and below 
the end of the root. 

Fig. 48 illustrates the alveolar border on the right side of 
Fig. 45, greatly amplified. This shows the progress of intersti- 
tial gingivitis extending through the alveolar process producing 
absorption with intense inflammation of the peridental mem- 
brane and abscess with fistulous tract. 

Fig. 49 shows a similar process amplified from the left side of 
Fig. 47. It is interesting to note in this illustration that the 
fibers of the sub-epithelium pass down and become interwoven 
with the coarser fibers of the periosteum in just the opposite 
direction from those in the other side of the tooth, and in other 



illustrations. The fibers from the mucous membrane along the 
side of the tooth extend down and into the peridental membrane 
without a break in the structure. The arrangement of the fibers 
of the submucous layer in producing the fold is well illustrated 
in the figure. This picture illustrates inflammation starting in 
the gingival border. 


To secure a chain of evidence that interstitial gingivitis (due 
to the metals, drugs, uric, lactic and other acids) commenced in 

Proj. % inch, ocular I 1 /.- inch. Spencer. 

Fig. 50. — Longitudinal Section of Gingival Border, Showing Round-Cell. 
Inflammation Due to Mercurial Poisoning. 

the papillary layer of the sub-epithelial, mucous membrane, I 
instituted a series of experiments in mercurialization of dogs. 
Dogs for the purpose were picked up in the streets. Some 
of these were operated upon by myself, but most of them were 
under treatment at the Post-Graduate Medical School. Care 



was taken to secure those in health and with healthy gums. 
Mercury was introduced by the mouth, skin and hypodermic 
injection. It was no easy matter to get them under influence 
of the drug, since the power of the glands to eliminate the poison 
was enormous. In no case was salivation produced. The first 
symptom noticed was exhilaration, which would last from three 
days to a week. Then paralysis agitans would continue until 
death. In about a week the appetite would commence to fail 
and it was difficult to get the dogs to take food of any kind. 
The kidneys and bowels eliminated the poison. There was a 

Pantaehr. oil 

No. 3. Leitz. 

Fig. 51. — Longitudinal Section op Gingival Border. Higher Magnification, 
Showing Connective Tissue Infiltration with Plasma Cells and Polynu- 
clear Leucocytes. Dog. 

rise in temperature. Some of the dogs died before gingivitis 
was observed. This demonstrated that not only does the nervous 
system become involved, but the organs of the body may be 
morbidly affected and death ensue before the gums show symp- 
toms of disease. Some dogs were killed after the gums became 



diseased. The time required to obtain results was from three to 
eight weeks. The age and physical condition of the dog caused 
this variation in time. After death the gum tissue was dissected 
from different parts of the jaws and placed in either fifty per 
cent alcohol, Muller's fluid, or two per cent formalin. 

Sections of tissue from the gum margin and sides were made 
on a number of places. Some were imbedded in paraffin, others 
in celluloidin. The sections were stained according to various 

Pantaehr. oil imin. 1/12 inch ocular. No. 3. Leitz. 

Fig. 52. — Longitudinal Section of Gingival Border. Higher Magnification, 
Showing Round-Cell Inflammation Extending to the Inner Coat of the 
Blood Vessel and also Plasma-mast Cells. 

methods: Delafield's hematoxylin, eosin (Unna's), alkalin 
methylblue, carmin, Gramm's stain, etc. 

Microscopic examination showed that the epithelial lining of 
the gums did not present pathologic changes, but appeared nor- 
mal in every respect. Connective tissue below the gum epithe- 
lium (the tissue analogous to the papillary layer of the derma 
and the derma proper) presented unmistakable evidences of a 



mild inflammatory process. There occurred in this connective 
tissue round-cell infiltration, generally moderate but in some 
places quite dense. This cellular infiltration extended from 
below (where it was densest) upward into the papillary layer 
(Figs. 50 and 51). The densest cellular infiltration usually oc- 
curred around the vessels (Fig. 51). 

Under high magnification, the cellular infiltration was found 
to consist of polymorphonuclear leucocytes, plasma cells and 

Projection % inch, ocular 1% inch. Spencer. 

Fig. 53. — Longitudinal Section of Gingival Border, Showing Round-Cell Infil- 
tration in the Connective Tissue and Extending into the Papillae. Dog. 

plasma-mast cells, the latter with coarse basophilic granulations 
(Figs. 52 and 53). 

In some places were seen between the round cells, short, 
broad fusiform cells, the protoplasm of which took quite well 
basic methylblue. These cells resemble very much fibroblasts 
and appear to be derivations of the plasma cells (Fig. 54). No 
bacteria were found either in the areas of cellular infiltration 
(inflammatory areas) or elsewhere. In these cases it is obvious 



Pantaehr. oil imm. ] /12 inch ocular. No. 3. Leitz. 
-Longitudinal Section of Gingival Border, Showing Round-Cell Inflam- 
mation Due to Mercurial Poisoning. Higher Magnification. 

Fig. 55. 
A monkey skull showing absorption of the alveolar process (original). The right 
central and left lateral have dropped out. The alveolar process is absorbed so 
that all teeth are loose. 

MKi;cri;iAL ixtkkstitial <;rx<;ivrns in 

1 55 

that there had occurred a mild inflammation of the gums (gingi- 
vitis). While this could not be seen with the naked eye, micro- 
scopic examination demonstrated histologic features of an in- 
flammatory process. The absence of bacteria justified the 
belief that this inflammation was not of microbic origin, but due 
to mercury, which by its well-known chemotactic influence pro- 
duced the histologic changes of an inflammation. 

Fig. 55 is the skull of a monkey who died aged one year of 
tuberculosis. Absorption of the alveolar process is the result 
of autointoxication acting upon a depleted organism. The right 
superior and inferior central and lateral incisors have loosened 
and dropped out. The roots of all the teeth are exposed to a 
marked extent. The teeth could be removed with the fingers. 




While hundreds of slides could be adduced in support of this 
chain of evidence, sufficient have been given to permit of the 
introduction of evidence from other phases of the subject. 

The following autopsy was made by L. Hektoen on an old 
man, in whose case the pathologic diagnosis was as follows: 
Senile marasmus (senile emphysema, senile sclerosis of the 
aorta, atrophy of the parenchymatous organs), scurvy (hemor- 
rhagic gingivitis); chronic aortic and mitral endocarditis; 
fibrous myocarditis; chronic nephritis; caseo-calcareous areas 
in the right apex, spleen and left adrenal ; double hydrothorax ; 
bronchitis ; fibroma of the stomach ; amputation of the left lower 
extremity at the lower third of the thigh. The findings unre- 
lated to the scope of the present investigation are omitted. The 
gums were found swollen, and here and there infiltrated with 
blood. There was purulent matter about the roots of the teeth, 
many of which were loosened and some of which could be 
removed with the fingers. The roots of the loosened teeth were 
covered with a granular grayish material. 

Bacteriologic examination of the root of the tooth gave the 
following results : Tube of bouillon from which agar plates 
were made, inoculated twenty-four hours before date, July 29, 
1898. There were two varieties of colonies: Both grayish 
white. One kind is round, pin-head size, slightly elevated, with 
thin, wavy, but sharply defined border. Finely granular. Media 
inoculated from one of these. Agar Slant: White, tallow- 
like growth along the track of the needle, with thin, more trans- 
lucent layer covering the rest of the surface. Only moderately 
elevated. Greenish tinge given to media. Potato: Elevated, 
"clumpy" growth, white on top, confined to needle track. 
Potato much darkened. Blood Serum: Gray, waxy growth, 
little elevated, sharply defined and thick border. Gelatin Slab: 
Saucer-shaped liquefaction at upper part, more tubular in deeper 


portions. Flocculent masses throughout. Glucose Agar: Gas 
produced, white, thick growth on top. Milk: Alkaline, soft 
coagulation. Bouillon: Cloudy. Characteristics: Rapid growth, 
a sour, nauseating odor given off from all media. Morphology: 
Large coccus, single, in pairs and in groups. Stains easily by 
ordinary methods, also by drams. The smaller colonies on agar 
plates (pin-point sized in center) with nearly transparent, illy 
defined peripheral zone. Border indistinct. Central portion in 
gray. Finely granular throughout. Agar Slant: Gray film 
over entire surface, somewhat thicker along the inoculation 
streak. At bottom there is a nearly white growth. Very light, 
greenish tinge to media. Blood Serum: Like on agar. Potato: 
Heavy dirty gray growth, wavy and sharply defined border. 
Looks like bunch of cauliflower. Gelatin Slab: Liquefied, 
saucer-shaped at top, tubular in deeper part. Growth mostly 
in upper stratum. Lit. Milk: Negative. Bouillon: Cloudy. 
Glucose Agar: Gas produced. Characteristics: Rapid 
growth, stinking odor from all media. Morphology: Small, 
slender bacilli; actively mobile, spores. "Takes ordinary stains 
readily and is not decolorized by Gram's method. 

Only the lower frontal teeth and corresponding part of the 
jaw could be examined. The epithelial covering of the gums 
appeared to be quite intact. In some places it was a little thick- 
ened, and its lower layers infiltrated with new cells. The sub- 
epithelial tissue was much thickened, presenting the general 
structure of an inflammatory granulation tissue of some stand- 
ing. Areas occurred in which there were many new cells and 
but little stroma. In other foci the tissue was more fibrous, the 
new cells running in bands. Here and there occurred free and^ 
intracellular granular, yellow pigment. Typical hyaline bodies 
of various sizes, and staining a precise bluish violet with Gram's 
method, were found in rather small numbers. In some places 
small sub-epithelial abscesses were met with, which (in the 
instance of a district including a lower incisor) were really sub- 
periosteal. The contents consisted of nuclear detritus and bac- 
teria (mostly cocci) which have accumulated, especially upon 
and in the walls of the minute cavities extending from such an 
abscess. There seems to be a complete occlusion of the vessels 

X 40. 35 M. M. Zeiss. Micro-photograph, reduced one-third. 

Fig. 56. — Longitudinal Section of Tooth, Alveolar Process and Gingival Border, 

Showing Active Inflammation in Scurvy in Man. 

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. 
H, Periosteum. J, Alveolar Process. L, Haversian Canals. M, Fibrous Tissue. V, 
Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Mem- 
brane. BR, Space Pocket from Want of Union of the Epithelial Fold. 

X 40. 3.3 M. M. Zeiss. Micro-photograph, reduced one-third. 

Fig. 57. — Longitudinal Section of a Tooth, Alveolar Process and Gingival 
Border, Showing Active Inflammation in Scurvy in Man. 

B, Dentine. C, Cementum. E. Epithelial Tissue. <;. Submucous Membrane. 
V, Violent Inflammation. Z, Sloughing of the Epithelial Tissue Due to Calcic Deposits. 
AA, Point of Union of Epithelial Tissue and Peridental Membrane. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 58. — Longitudinal Section of Tooth, Alveolar Process and Peridental Mem- 
brane, Showing Blood Pigment in Blood Vessels of Peridental Membrane 
in Scurvy in Man. 

C, Cementum. 

J, Alevolar Process. K, Capillaries. I 1 , Inflamed Peridental Mem- 
brane. K l , Blood Pigment in Capillaries. 

X 7.". A. A. <iiij. Zeiss. Micro-photograph, reduced one-third. 

Fig. 59. — Longitudinal Section of Tooth and Gingival Border. Showing Active 
Inflammation Extending through the Mucous and Peridental Membranes. 
Scurvy in Man. 

B, Dentine. C, Cementum. E, Epithelial Tissue. V, Violent Inflammation. AA, 
Point of Union of Epithelial Tissue and Peridental Membrane. KR, Space Pocket 
from Want of Union of Epithelial Fold. M\ Inflamed Fibrous Tissue. 


(capillaries) with typical bacteria masses, staining a peculiar 
bluish violet color with hematoxylin, and blue with Gram's 
method, so that the vessels presented the appearance of being 
very successfully filled by an infection mass : the small dilata- 
tions, the branches and the larger vessels (judging from struc- 
ture these seemed to be veins) were sometimes brought out very 
nicely. The intravascular growth of bacteria extended into the 
bone below as well as, and more especially into, the peridental 
membrane. 1 These abscesses (suppurative periostitis) occur 
almost exclusively upon the inner surface of the alveolar proc- 
ess, being confined (as far as there was occasion to observe) to 
the external aspect of the process. There was always a thin, 
sound layer of bone separating the abscess from the peridental 
membrane. Very generally the spaces in the adjacent bone 
were filled with a cellular fibrous tissue in which occurred islands 
of osteoid tissue. The bone trabecular were generally covered 
by a thin layer of osteoid tissue, which (from the greater num- 
ber of cells it contains, as compared with the other bones) must 
be newly formed. Rows of osteoblasts were found often upon 
the trabecular Few Howship's lacuna? were found, and these 
were filled with small cells. There were no osteoclasts in the 
areas about the abscesses. The bone outside of the alveolar 
process was quite unchanged. 

The "bacterial thrombosis" not unusually extended into the 
peridental membrane, which then refused to stain as clearly as 
normal. The upper part of the peridental membrane was 
usually the seat of cell proliferation, and of the formation of 
fibrous tissue, due to the direct extension of the similar process 
in the sub-epithelial connective tissue of the gingivus. There 
were no indications that the process began below, at the apex of 
the tooth, for example, and extended upward. In the peridental 
membrane, and often connected with the cementum of every 
tooth examined, were very many so-called calcospherites ; cal- 
cified, concentrically lamellated, round or oval bodies, not unlike 
the "corpora amylacea." In many instances, it seemed as if the 

1 The abscesses have a definite outline or wall of ordinary cellular fibrous tissue 
displaying striking evidences of active inflammation. The tissue about the capilla- 
ries filled with bacteria refuse to stain clearly, but there are no signs of inflammation. 


body had formed in the cement or at its margin — the cement 
presenting- here a nodular condition. 

Fig. 56 illustrates a section through the tissues of the jaw 
and cuspid tooth. The epithelium is not so dense and thick as 
in a similar section from the dog. Inflammation extends along 
the papillary layer of the submucous membrane (G) and involves 
the deeper structures. The mucous membrane layer has doubled 
upon itself, forming a pocket (RE). Violent inflammation is 
evident at V. This is of unusual interest, since it demonstrates 
that inflammatory products may be carried by the blood vessels 
anywhere throughout the alveolar process, and may result in 
abscesses. The inflammation extends throughout the periosteum 
(H), the fibers of which extend from the root of the tooth over 
the border of the alveolar process (J). There the coarse fibers 
of the periosteum contrast decidedly with the finer fibers of the 
sub-epithelium. Absorption and contraction of the alveolar 
process (fully one-half the length of the root of the tooth) has 
taken place, as well as lateral absorption. The inflammatory 
process extends through the Haversian canals (L). 

Fig. 57 is a section through the jaw at the lateral incisor. 
The epithelium (E) is seen upon the outer surface of the alveolar 
process as far as the root of the tooth. The inner fold next to 
the tooth has disappeared through encroachment of deposits 
which have been destroyed by nitric acid. Inflammation ex- 
tends throughout the entire submucous membrance (G). The 
most marked inflammation in this case is entirely upon the 
outer border (V). 

Fig. 58 shows a section of the peridental membrane (I) 
and alveolar process (J). Capillaries (K) interlace through 
the field, the largest number being distributed along the 
alveolar wall. Blood pigment containing bacteria is notice- 
able (K'). 

Fig. 59 is an amplification of a section depicted in Fig. 56. 
This gives a clearer idea of the folding of the epithelium (E) 
and submucous membrane (G) layer upon itself, forming a 
pocket (RR), in which may be seen an accumulation of food and 
bacteria. It also shows extensive inflammation throughout the 
entire field. Marked inflammation is evident at V. The point 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 60. — Cross Section Peridental Membrane, Showing Active Round-Cell In- 
flammation. Scurvy in Man. 

C, Cementum. V, Violent Inflammation., W, Epithelial Debris. EO, Endar- 
teritis Obliterans. 

X 75. A. A. obj. Zeiss. Micro-photograph. reduced one-third. 

Pig. 61. — Cross Section* of Inflamed Peridental Membrane. Scurvy in Max. 

I, Peridental Membrane. J. Alveolar Process. K, Capillaries. L, Haversian 
Canals. BR, Blood Vessels of \'<m Ebner Preceding Perforating Canals. EO, Endar- 
teritis Obliterans. W, Epithelial Debris. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 62. — Cross Section of Tooth, Alevolar Process and Peridental Membrane, 
Showino Active Inflammation and Absorption of Bone. Scurvy in Man. 

C, Cementum. I, Peridental Membrane. J, Alveolar Process. P, Perforating Canal 
Absorption. V, Violent Inflammation. 



j . v3§s 

u. 'H 

>l V.- i 

l 4 


^^„. ^w 

^^ B jr^^kfwr^'^ ""■**■*' 



N**-^^- rf^jP 




s * s ^5?*.~ 



X 40. 35 M. M. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 63. — Cross Section op Peridental Membrane and Alveolar Process, Showing 
Active Inflammation and Abcess. Scurvy in Man. 

J, Alveolar Process. T, Bacteria. Y, Abcess. P, Inflamed Peridental Membrane. 
L, Inflammation Extending through Enlarged Haversian Canals. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 64. — Cross Section of Peridental Membrane and Alveolar Process, Show- 
ing Active Inflammation and Another Larger Abcess. Scurvy in Man. 

J, Alveolar Process. P, Perforating Canal Absorption. V, Violent Inflammation. 
Y, Abcess. I 1 , Inflamed Peridental Membrane. L 1 , Inflammation Extending through 
Enlarged Haversian Canals. 



of union of the sub-epithelial layer and the periosteum is shown 

Fig. 60 illustrates inflammation of the peridental membrane 
with epithelial debris (W) scattered over the field. Endarteritis 
obliterans (EO) is also noticed at various positions. Marked 
inflammation may be seen at V. 

Fig. 61 illustrates a section of the peridental membrane (I) 
and alveolar process (J) with inflammation extending through- 
out. Capillaries (K) are also noticeable in large quantities, 

X 300. Xo. 2 projection ocular. D. T>. obj. Zeiss. 

Fig. 65. — Cross Section op Tooth, Alveolar Process and Peridental Membrane, 
Showing Active Inflammation with Calcospherite in Membrane. Scurvy 
in Man. 

B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. 
HH, Calcospherite. J 1 , Inflamed Peridental Membrane. L 1 , Inflammation Extending 
through Enlarged Haversian Canals. 

nearer the alveolar process than the root of the tooth. Epithe- 
lial debris is evident at W. Endarteritis obliterans (EO) may 
be seen in different portions of the field. Inflammation has 
extended into the Haversian canals (L) but absorption has not 



occurred to any great extent. The blood vessels of Von Ebner 
(BB) are quite well shown. 

Fig. 62 is a section showing the cementum (C), the peri- 
dental membrane (I) and the alveolar process (J). Marked 
inflammation extends through the peridental membrane, thence 
through the Haversian canals (which are entirely obliterated). 
Absorption of the trabecular (halisteresis) has resulted to the 
extent that what remains of the alveolar process (J) are islands 
of bone held in place by the fibrous tissue. Blood vessels of 
Von Ebner with perforating canals are seen at P. 

Fig. 63 shows a section of the peridental membrane and 
alveolar process with a large abscess originally within the 
alveolar wall. Inflammation spreading through the peridental 
membrane has occurred at I', while the decalcified alveolar 
process is also shown (J). Violent inflammation has taken 
place within the alveolar wall, and an abscess (Y) has formed. 
The wall of the abscess is distinctly seen, with masses of bac- 
teria (T) clinging to the inner sides. The process of halisteresis 
(Q) (bone decalcification) is seen as a result of the violent 
inflammation. The entire wall next to the peridental membrane 
and about the abscess has been destroyed, and the different 
stages in the process by which this has been accomplished are 
beautifully shown. 

Fig. 64 illustrates a larger abscess (Y) from another loca- 
tion. This is also situated within the alveolar wall, showing 
that the inflammatory products extend through the blood ves- 
sels. Marked inflammation is seen upon the side next to the 
peridental membrane (Y), while rapid absorption — halisteresis 
(Q) and perforating canal (P)— is proceeding at the borders 
of the abscess and nearest the alveolar process. 

Fig. 65 shows a section of a tooth (B and C), inflamed 
peridental membrane (Y), with absorption of the alveolar proc- 
cess (J). In the inflamed peridental membrane may be seen 
a calcospherite, oblong in form. 


A forty-eight-year-old merchant was dyspeptic, debilitated 
and asthmatic, and for the treatment of these conditions he had 
been under calomel and tonics for a little less than two weeks. 


When he came under observation, the mucous membrane and 
gums were then much inflamed. There was marked sialorrhcea. 
The teeth were loose. The gums were swollen. Pus oozed from 
the gums. The breath had a decided metallic odor. At my sug- 
gestion, his medical attendant stopped the calomel. He was 
then ordered six pints of spring water daily. The gums were, 
on alternate days, saturated with iodin. In a few days the sore- 
ness and swelling were so reduced that the deposits could be 
removed. The patient was discharged cured in a short time 
other than as to the right inferior second molar, which was so 
loose as to require removal. This tooth was placed immediately 

Fig. 66. — Shows a Small Fragment of [nflamed Peridental Membrane. 

in fifty per cent alcohol for twenty-four hours and then removed 
to absolute alcohol for twenty-four hours more. The membranes 
had receded about two-thirds the length of the root. Sections 
for microscopic purposes were made from the lower third of the 
root. Of these sections, Fig. 66 shows a small fragment of in- 
flamed peridental membrane. Fig. 67 exhibits violent round-cell 
inflammation, degeneration and liquefaction of tissue. 

A thirty-five-year-old diabetic painter came under observa- 
tion for plumbic poisoning. His gums were swollen. There was 
decided sialorrhcea. The teeth were loose. Pus flowed from the 
gums. He was placed on ozonate spring water and the gums 



were saturated with iodin on alternate days. Three loose teeth 
were removed and placed in alcohol. Sections from the upper 
third of the left superior second bicuspid gave results on micro- 
scopic examination similar to those already described as occur- 
ring in mercurial poisoning. Fig. 68 shows round cells of in- 
flammation. Fig. 69 illustrates very marked degeneration of 
the peridental membrane. In the lower right-hand corner are 
seen the root of the tooth, dentine and cementum. The whole 
surface of the peridental membrane is in an advanced phase of 

-Violent Bound Cell Inflammation, Degeneration and 
llquification op tissue. 

inflammation. Just at the border of the root is evident an area 
of membrane softening. Just beyond, but joining, is noticeable 
breaking down of tissue. In the center are seen two areas of 
softened tissue more advanced in degeneration. 

One occupation disease which has been ignored in the etiology 
of interstitial gingivitis is ' ' brass-workers ' ague. ' ' In almost all 
brass-workers, a stain varying from a bright to a brownish green 
is detectable on the necks of the teeth between the crowns and 



the gum insertion. This is most obvious in the upper jaw. 
After a while, as E. Hogben 2 has shown, the teeth become 
loosened and fall out. Before these changes in the gum occur 
nervous symptoms have developed from the brass poisoning. 

Arsenic should be taken into account in the etiology of inter- 
stitial gingivitis. This drug has a very decided tendency in cer- 
tain subjects to cause, even in small doses, marked stomatitis 
and irritation of the mucous membranes throughout the body. 

Tartar emetic and the other preparations of antimony, pro- 
ducing irritation of the mucous membranes of the mouth and 
elsewhere, may act as predisposing and exciting factors of inter- 
stitial gingivitis. 3 

Fig. 68. — Section of Pericemental Membrane Showing Round Cell Inflammation. 

Among the drugs which should be taken into account in the 
etiology of interstitial gingivitis is potassium bromide. This 
produces in certain individuals, or when given to excess, marked 
increase of the saliva with irritation of the mucous membranes 
of the mouth, followed later by dryness of the mouth and shrink- 
ing of the gums. The bromides have, as H. C. B. Alexander * 
has shown, a tendency to irritate all the mucous membranes of 
the body as well as the skin. Therefore, in dealing with cases 

Birmingham Medical Review, 1887. 
Lewin: Untoward Effects of Drugs. 
Alienist and Neurologist, July, 1896. 



of interstitial gingivitis in which the bromides are being taken, 
this factor should not be neglected. In these cases the symptoms 
due to the bromides are apt to be charged to the nervous state for 
which the bromides have been given. The irritation of the 

mucous membrane by the bromides may occur quite early among 

-Marked Inflammation and Degeneration of the Peridental 
Showing Four Peridental Abscesses. 

the untoward effects produced by them. In all probability the 
bromide rather than the alkali is the source of these untoward 

What is true of the bromides is also true to an even greater 
degree, as has elsewhere been shown, of the iodides. 



Referring- to Chapter VI we find that the peridental mem- 
brane is a fibrous tissue situated between the root of the tooth 
on the one hand and the alveolar process on the other. It covers 
the root of the tooth. This structure, to all intents and pur- 
poses, is a continuation of the trabecular or fibrous tissue in the 
alveolar process. In other words, the alveolar process is noth- 
ing more or less than fibrous tissue filled in with lime salts. 

If a piece of jaw containing teeth be placed in a weak acid 
solution and the lime salts dissolved, there would be no distinc- 
tion, under the microscope, in the remaining structure from the 
root of the tooth to the outer surface including the periosteum 
except in quality of fibers. When a low form of inflammation is 
set up in the alveolar process, the lime salts are absorbed, leav- 
ing the fibrous tissue in like manner. If on the other hand, the 
inflammation is more intense, the trabecular or fibrous tissue is 
also destroyed. 

Irritations of a local nature first produce a gingivitis of the 
gum tissue which extends along the blood vessels into the deeper 
tissues and assumes an interstitial character. "When the irrita- 
tions are constitutional, due to autointoxication, drug, or other 
irritation and poisons, the deeper tissues become involved, then 
assuming an interstitial character, later affect the gums, pro- 
ducing gingivitis. When the peridental membrane becomes in- 
volved, whether from local or constitutional causes, it is termed 
pericementitis. This disease is always recognized by soreness 
and a slight elongation of the tooth or teeth. 

If the cause be slight or if removed, the membrane mil re- 
turn to its normal condition. On the other hand, if the cause be 
severe and of long standing the inflammation will become 
chronic, resulting in absorption of the alveolar process and per- 
haps abscess. 


A low form of pericementitis may act upon the surrounding 
tissues in different ways, depending, to a great extent, upon the 
nervous system. First, if there are no corresponding teeth for 
antagonism on the opposite jaw, the inflammation will cause a 
deposition of lime salts in the alveolar process, causing elonga- 
tion which continues until the tooth or teeth meet resistance. 
Second, exostosis of the cementum of the tooth. Third, the 
inflammation results in peridental or alveolar abscess. Later, 
especially if the irritation be of a constitutional nature, the 
inflammation will cause absorption of the alveolar process and 
exfoliation of the teeth. 

A seamstress bites her thread, pericementitis results. If 
treatment be resorted to and the habit stopped, the peridental 
membrane will be restored to health. If, however, this habit 
be continued, interstitial gingivitis results, with absorption of 
the bone and loosening of the teeth. The habit of biting threads 
with the teeth causes an extra amount of work upon the peri- 
dental membrane. Persons suffering with autointoxication 
would naturally find such teeth first involved in interstitial 
gingivitis. The same results follow when a low form of inflam- 
mation occurs in the three classifications just mentioned above. 
Persons of low vitality, poorly nourished people suffering with 
prolonged sickness and pregnant women have periostitis and 
general interstitial gingivitis. Persons overworked or suffering 
with neurasthenia are prone to it. 

In syphilis, pericementitis and interstitial gingivitis are set 
up and not only in the alveolar process, but all bones of the body 
may become involved, causing hypertrophy as well as absorp- 
tion and death of bone. Heat and allied irritation will produce 
interstitial gingivitis and bone absorption. 

Some more severe forms of pericementitis and interstitial 
gingivitis deserve attention from the irritation point of view. 
I have for years moved the teeth of dogs with regulating appli- 
ances, using a screw with sixty threads to the inch. In some 
the screw was turned one-fourth round, in others one-half, and 
in still others one full turn once a day. Some of the dogs were 
killed in three days, others in a week, and still others in two 
weeks. By this method the simplest and most severe forms of 

iiksk \iri 1 1 i:s ( >x nr.MA.x ix peuickmextitis. 


pressure were applied, the length of time being brief as well as 
extended. These tissues were decalcified, cut, stained and 
mounted for the microscope. In every case inflammation of the 
pericementum was produced. This disproves the theory so long 
held, that bone absorption in regulating teeth is purely a physio- 
logic process. Teeth were also extracted from dogs and after 
a week they were killed. The bone was decalcified, cut, stained 
and mounted for the microscope. The absorption was inflamma- 
tory in character. The jaws of dogs and monkeys who were 
erupting the permanent teeth were treated in like manner. Ab- 

FlfiURE 70. 

Inflammation of the gum margin (original). 

sorption of the alveolar process to allow the teeth to pass into 
position was of inflammatory type. Simple irritation, as well as 
severe pressure, hence produces the same pathologic process, 
pericemental inflammation and interstitial gingivitis. 

The blood vessels which supply the gums, pericemental mem- 
brane and alveolar process are, as I have elsewhere demon- 
strated closely connected. Those in the pericemental membrane 
form a plexus along the wall of the alveolar process, while only 
a small number are near the roots of the teeth. So closely con- 



nectecl are these that the vessels in one cannot become involved 
without affecting those of the other tissues. Hence, gingivitis 
and pericementitis occur which in reality become interstitial, 
or interstitial inflammation appears, which in reality becomes 
gingivitis. No matter what the cause may be, or whether the 
initial lesion be in the gum or interstitial structure, absorption 
of the alveolar process eventually results. 

I began my experiments upon the peridental membrane in 
1896. In 1897, I read an article before the Section on Stoma- 
tologv of the American Medical Association, demonstrating the 

Figure 71. 

Section deeper at the alveolar border (original). Active inflammation around two 
arteries which are becoming thickened. 

pathology of the peridental membrane from simple inflammation 
to the breaking down of tissue and the formation of abscess. 

A bicuspid tooth with a gold crown attached was taken from 
the mouth of a fifty-four-year-old man. He was suffering from 
autointoxication and neurasthenia. The tooth had become quite 
loose although the gum tissue was still intact. The irritation 
was both local and constitutional in character, since the gold 

i;hsk\i;< iii;> <>x iiiwian in i>ki;ici-:.m k.X'i Ti'is. 


crown irritated the gum margin and a slight attack of Bright 's 
disease caused self poisoning. 

The following illustrations are taken from microscopic slides 
and magnified four hundred and eighty diameters. Fig. 70 
shows the gum tissue. The epithelial layer shows the dipping 
down of the legs into the true mucous membrane below the base- 
ment membrane, with round cell infiltration due to irritation. 
Fig. 71 is a cross-section of peridental membrane of the left 
inferior central incisor of a lady twenty-nine years of age who 

Figure 7D. 
Active inflammation in peridental membrane and trabecular (original). 

had been under my care for fourteen years. She was in the 
habit of biting her thread with this tooth. Her occupation, that 
of dressmaking, gave her little or no exercise and she was also 
overworked. She drank no water ; she was suffering from sleep- 
Lessness and nervousness due to indigestion and autointoxica- 
tion. Sections of tooth, after decalcification, were made in the 
usual manner for the microscope. A cross-section shows two 
blood vessels which are considerably thickened (endarteritis 
obliterans) in its early stages with round cell infiltration in the 
tissues about them. 



Figure 73. 
Violent inflammation in the peridental membrane and trabecute (original). 

Figure 74. 

Shows the root of the tooth, the peridental membrane, active inflammation in the 
trabecule and the formation of two abscesses. Note that both these abscesses are 
located in what was once the alveolar process. The peridental membrane can be 
readily observed between the root of the tooth and the nearest abscess (or- 


The preceding three illustrations show the different stages of 
inflammation and liquefaction of the peridental membrane of the 
right superior first molar in a forty-year-old lady, a marked 
neurasthenic who has had periostitis and interstitial gingivitis 
with pyorrhoea alveolaris for the last twenty years and is now 
losing her teeth very rapidly. Fig. 72 shows a cross-section of 
palatal root near the apex, showing active inflammation in the 
peridental membrane. The round cell inflammation with exudate 
is rapidly collecting between the bundles of connective tissue 
fibers. Fig. 73 is a cross-section of the same root nearer the 
apex showing connective tissue with active inflammation, a stage 
further advanced than that of the previous illustration. In this 
area no fibrous tissue can be seen. Fig. 71 shows a still further 
advance in degeneration and liquefaction, forming an abscess. 
This is a lower magnification, showing a portion of the two 
buccal roots of the tooth, peridental membrane and the trabecule 
or fibrous tissue which was once alveolar process between them. 
The peridental membrane may easily be distinguished around 
each root from the trabecular between them. Two areas of 
softening and liquefaction may be seen forming two abscesses. 



The local irritations producing interstitial gingivitis are the 
eruption of the teeth, change in function, tartar, uncleanness, 
lactic acid ferment, irritations due to modern dentistry, irreg- 
ular teeth, regulating teeth, implantation of teeth. 

Many years ago 1 I stated that modern dentistry was one of 
the most fruitful sources of interstitial gingivitis. Irritations 
from foreign substances, such as detached bristles of the tooth- 
brush, too great friction in brushing the gums and alveolar proc- 
ess, where the latter is prominent, injudicious use of the tooth- 
pick, the use of ligatures in holding in rubber dam and regulat- 
ing teeth, regulation of teeth with any applicance, application of 
the rubber dam, the use of clamps, crown and bridge work, irri- 
tation and heat due to artificial dentures and regulation plates, 
overlapping fillings, injuries from instruments, the devitaliza- 
tion of pulps, root fillings which throw increased work upon the 
peridental membrane or irritate it, in a word whatever irritates 
the gum margin, peridental membrane or alveolar process, is 
likely to produce inflammation which later becomes chronic. I 
am convinced that the disease is contagious, or progressive, not 
from one individual to another, but from one tooth to another in 
the same mouth. 

The greatest and most important local cause of interstitial 
gingivitis is that of the eruption of the teeth since nearly every 
person possesses two sets. 

Tooth eruption of both the first and second set ushers in the 
second and third periods of stress. It is at these periods when 
great changes take place in the system of the child and mark 
the early eras of future welfare. The absorption of bone in the 
eruption of the teeth and the building up of bone about the roots 

Talbot, The Dental Cosmos, Nov. 1886. 


to hold them in place is an inflammatory process. How well this 
is accomplished depends upon the health of the child. In neu- 
rotic and degenerate children, when the nervous system is un- 
stable and the child's vitality is of low order, the process of 
absorption and deposition of bone cells is not carried on nor- 
mally. Especially is this true in the building up of the alveolar 
process about the roots of the teeth. Interstitial gingivitis re- 
mains in the alveolar process to a greater or lesser extent during 
the entire period of and until the shedding of the first set of 
teeth. The extreme illustrations of this disease are those con- 
nected with rachitis, infantile scurvy, inherited syphilis, marked 
neurosis, degeneracies and similar diseases. The jaws are often 
small, the alveolar processes are undeveloped and quite loosely 
built up. The gums are always inflamed and frequently ulcer- 
ated. At the second period of stress, when the first teeth are 
erupting the entire alimentary canal as well as all the internal 
organs undergoes changes in preparation for the reception of 
solid starchy food. The effects upon nutrition at this time are 
severe. In every patient there is more or less inflammation in 
the alveolar process, gums and peridental membrane until the 
first teeth are shed. 

When the second set of teeth erupt there is a double inflam- 
matory process going on in the tearing down of the bone to 
remove the temporary teeth and building up the process for the 
permanent teeth. So irregular is this action that in many 
mouths there is a continuous inflammation through the entire 
process on both jaws. This is noticeable in neurotics and de- 
generates and in those children whose vitality is low and who 
are' poorly nourished. The bone is porous and loosely put to- 
gether. The severity of interstitial gingivitis during the erup- 
tion of both sets of teeth and after all of the second teeth are in 
the mouth will depend upon the nervous system and blood sup- 
ply. It must not be lost sight of, that, after all of the second set 
of teeth are in the mouth, there is a restlessness existing among 
them till all are securely located in their respective localities, 
although they may not be in their proper relations to each other. 
As long as this restlessness continues, and it may persist until 
middle life, interstitial gingivitis is always present. The irri- 


tation set up by the advancing teeth causes inflammation in the 
gums and alveolar process. A visit to schools for defective chil- 
dren and an examination of their mouths will convince any one 
of the truth of this statement. 


Change in function has been discussed in a general way in 
previous chapters. It is necessary, however, to state here that 
owing to use and disuse of structures and environment, the func- 
tion of mastication is gradually being reduced to a minimum. 
On this account and the gradual reduction of the size of the jaws 
and straight crowned teeth, the alveolar process, has, in most 
persons, changed its shape and has become narrow, long and 
thin. This change in shape and loss in blood and nerve supply 
makes the process about one or more teeth exceedingly suscep- 
tible to disease and destruction on account of loss of function. 


Tartar is the excess of lime salts in the blood excreted 
through the salivary glands. It remains soluble in the saliva 
until it reaches the mouth cavity when it precipitates. Just how 
precipitation is accomplished has not been proven beyond a 
doubt. One theory is that the action of ammonia exhaled from 
the lungs is the greatest factor. 

Kirk says, 2 "As the saliva contains carbon dioxid in solution 
it has been assumed with some justification, that the escape of 
the carbon dioxid which was the solvent of the calcium carbonate 
and tricalcic phosphate, causes a precipitation of those salts in 
the presence of the colloid mucin, in combination with which it 
deposits as tartar upon the teeth." 

H. H. Bouchard' proposed an explanation for the formation 
of salivary tartar deserving of consideration, viz., "that, 
inasmuch as fermentative processes in the oral cavity give rise 
to acids, and particularly lactic acid, these acids cause precipi- 
tation of the mucin of the saliva as a coagulum which entangles 
in its structure calcic phosphate and carbonate, and this mass by 

- Kirk. American Text-Book of Operative Dentistry, page 480. 

:: See Origin of Salivary Calculus by Henry H. Bouchard, Dental Cosmos. 1895, 
vol. XXVII, page 821. Also Varieties of Dental Calculi, by the same author, Dental 
Cosmos, 1898, vol. XL, page 1. 


gradual condensation increases in density to the extent of form- 
ing - the coherent deposit known as tartar." 

Tartar accumulations vary in quantity as well as in charac- 
ter in each individual and even in the same mouth. In some the 
greatest amount is found upon the molar teeth in opposition to 
the parotids whose function is apparently to keep the mouth 
moist. These glands constantly discharge small quantities of 
saliva without food stimulation. Owing to its special function, 
the sub-maxillary gland is stimulated by tasteful substances, 
hence probably does not send out as much lime salts. The sub- 
lingual glands next to the parotids discharge the greatest amount 
of calcic salts, which accounts for the quantity of deposit found 
on the posterior surface of the inferior incisors. The tartar will 
accumulate so rapidly in some mouths as to completely cover a 
tooth or teeth in a short time. In some autotoxic states there is 
always excess of tartar deposit. In a patient in whom mal- 
nutrition was most pronounced, deposits of tartar would collect 
so rapidly as to cover all the teeth in from four to six weeks. 
The teeth were of a degenerate type in that they had no enamel. 

In tartar analysis there is also great variation, that deposited 
near Steno's duct having the greater per cent of lime carbonate 
while that from the lower incisors has the greater per cent of 
lime phosphate. 

Tartar may be black, deep brown, green or yellow. In to- 
bacco users the deposit is usually black, presumably stained 
from nicotine. Other agents will stain tartar as w T ell. This is 
finely exampled in betel-nut chewers where "the rapid accumu- 
lation of large, dense deposits of tartar which at first are red, 
then finally become a dark, chestnut brown or black. ' ' 4 Nodules 
of tartar which cling with such persistency to the roots of the 
teeth are usually of a greenish or dark brown color and of great 
density. Tartar is not uncommon in domestic animals and the 
wild in captivity. I have no means of ascertaining whether wild 
animals running at large are thus affected. 

If the deposits of tartar are allowed to remain upon the 
teeth, they are added to day by day. Sooner or later, they set 

* Kirk. American Text-Book of Operative Dentistry. 


up irritation and inflammation in the gums, in the peridental 
membrane and in the alveolar process, with resulting interstitial 
gingivitis, pyorrhoea alveolaris and finally exfoliation of the 
tooth or teeth. 


Every one is familiar with the fact that those persons who 
possess small jaws and irregular teeth are more subject to inter- 
stitial gingivitis than those persons possessing normal jaws and 
teeth. This is due first to the fact that those persons possessing 
irregular teeth have unstable nervous systems. Second, the ir- 
regularity of the teeth brings the roots closer together, making 
the alveolar process thin between the roots, thus reducing the 
blood and nerve supply, and thus reducing resistance. The gums 
are inflamed from want of cleanliness and proper brushing and 
the function of proper mastication is lost. The gums thicken 
because engorged with blood and stasis takes place, resulting in 


One of the most fruitful sources of interstitial gingivitis is 
uncleanliness. Food and tartar collect on the teeth at the gin- 
gival border setting up irritation and inflammation. A want of 
proper measures for cleaning the teeth and gum margins after 
each meal soon allows the accumulation to irritate the gums 
which become inflamed and the food works its way along the 
roots of the teeth. The gums become inflamed, swollen and de- 
tached from the necks of the teeth. This condition allows more 
food and filth to collect which decomposes and forms lactic acid. 
This in turn also irritates the gums and further inflammation 


In my researches on interstitial gingivitis many years ago," 
I called the attention of the profession to the fact that modern 
dentistry was producing more inflammation of the gums, peri- 
dental membrane and alveolar process than any one cause. 
These irritations were most noticeable at that early period about 

5 Talbot. The Dental Cosmos, Nov. 


those teeth which had been "immediately separated for filling," 
so commonly practiced by the older members of onr profession 
before the rubber dam. A piece of orangewood made V-shaped, 
with the base resting upon the gum margin, was forcibly driven 
between the teeth for the purpose of obtaining plenty of room 
for immediate filling and also to press forcibly against the gums 
and alveolar process to prevent the gums from weeping, thus 
keeping the cavity dry. In the majority of cases so treated, 
interstitial gingivitis was set up which in time became chronic. 

The inflammation continued and followed the root upon one 
side oftentimes to the apex. The alveolar process became de- 
stroyed on the side of the inflammation and not infrequently 
pus infection would follow. The tooth would sometimes rotate 
upon itself or move in one direction or the other out of its posi- 
tion. The most excruciating pain accompanied the malleting 
of these wedges into place. 

The modern method of rapid wedging with separators is only 
a modification of this barbarous method of procedure and is fre- 
quently the source of interstitial gingivitis and later pyorrhoea 

Wedging teeth by any method sets up inflammation which 
may or may not be restored to normal. In any event, if poisons 
circulate in the blood later in life, such irritated or inflammatory 
localities, owing to the transitory nature of the structures, are 
the first to be affected by chronic interstitial gingivitis, since 
these structures have already been previously involved in struc- 
tural changes. 


The excessive use of the mallet which was necessary to build 
out teeth in those early days assisted greatly in producing in- 
flammation of the peridental membrane and alveolar process in 
connection with the rapid wedging. I recall a number of in- 
stances in my early practice where interstitial gingivitis and 
absorption of the alveolar process occured in neurotic children, 
the result of malleting in large gold fillings. These cavities were 
usually located in first permanent molars and sometimes in the 


bicuspid. Absorption of the alveolar process took place, the 
teeth became loose and dropped out or were extracted. 

At the present time malleting in large gold fillings in chil- 
dren's teeth, especially in neurotic, syphilitic, rachitic and sim- 
ilar children should be avoided on this account. The nerve 
strain, under such barbarous treatment, is very great and the 
boy or girl suffering from such constitutional conditions should 
be exempt from such procedure. 


When gold crowns were first introduced about 1880, the 
method of attachment was to drive the cutting edge of the gold 
to the alveolar process and disastrous results immediately fol- 
lowed. Inflammation set in and destruction of the alveolar 
process, with exfoliation of the tooth, soon followed. Since that 
time we have learned that gold crowns extending under the free 
margin of the gums will set up acute inflammation which after- 
wards becomes chronic and destruction of the alveolar process is 
sure to follow. 


When a bridge is placed upon two or more roots the function 
of those teeth has been destroyed. The teeth, owing to the elas- 
ticity of the jjeridental membrane, are allowed to yield slightly 
when pressure is applied in mastication. When they are bridged, 
they become rigid and the force of the impact in mastication 
irritates the membrane which together with autointoxication sets 
up further irritation and inflammation and absorption of the 
bone takes place. The collection of filth under bridgework is also 
a fruitful source of inflammation. Particles of food find lodge- 
ment under bridges and can not be dislodged by either tooth 
brush or toothpick. 


Destroying the pulps of the teeth and filling the roots throw 
extra work upon the peridental membrane. This extra work 
changes the normal function of the tissues. Poisons circulating 
in the blood cause an inflammatory process to first attack such 
teeth and rapid inflammation and absorption occur. 



Cavities at the margin of the gums and fillings with rough 
edges irritate the soft tissues and cause inflammation followed 
by absorption. 


Ligatures and clamps for holding the rubber dam not infre- 
quently irritate the gums and set up inflammation. 


Partial plates of any description for artificial dentures or 
regulating plates act as foreign bodies against the mucous mem- 
brane and gums, producing irritation by heat, by the accumula- 
tion of foreign substances beneath them and the edge of the plate 
will irritate the gums about the teeth, thus setting up inflamma- 


Not infrequently instruments used in excavating cavities, fin- 
ishing fillings, etc., will irritate the gum tissue which will later 
set up inflammation, absorption and finally destruction of the 


It is not uncommon to find teeth located on the external sur- 
face of the alveolar process. This occurs in those patients in 
whom the jaws are small for the long diameter of the teeth. The 
teeth in erupting will force their way into place and when in 
their normal condition the dental arch is located upon the outer 
border of the alveolar process. 

In such patients the bone over the roots of the teeth on the 
outside is often as thin as writing paper, while it is very thick 
upon the palatine and lingual side of the jaw. It is not uncom- 
mon to find the cuspid tooth located toward the outer side of the 
alveolar process while all the other teeth are in their proper 
places. The nerve and blood supply is almost nil, resistance or 
restoration is out of the question. 

Under such conditions too great stimulation by the tooth 
brush causes inflammation and absorption of the outer plate of 
bone, which in time will expose the roots of the teeth. 



The constant use of the toothpick, irritating the gum margin, 
is a fruitful source of interstitial gingivitis. This simple pro- 
cedure is a spendid illustration of the effect of slight irritation 
producing inflammation of the gum which later becomes chronic 
with eventual destruction of the alveolar process. 


One of the most prolific sources of interstitial gingivitis is 
the regulation of teeth. When we consider the nature of the 
alveolar process and what it is obliged to undergo by the time the 
permanent teeth have erupted and the sensitive condition in 
which it is placed as a transitory structure and end organ, after 
the permanent teeth are in place, together with the unstable 
nervous system of the patient, as well as the age at which this 
operation must be performed, the wonder is that after the oper- 
ation is complete there is any process left. 

The pressure necessary to move the teeth sets up an inflam- 
mation to produce the entire destruction of bone in line of pres- 
sure. A third set of teeth in our present phylogenic development 
is unnecessary and therefore nature is ill prepared, especially 
in neurotic children with unstable nervous systems, to again 
build up the alveolar process about the teeth. The degree to 
which the alveolar process will be restored will depend upon the 
condition of the nervous system, the blood and the age of the 
patient. If the patient is poorly nourished so that material (lime 
salts) is insufficient or the nerve supply to the part is unstable 
or the patient has obtained his growth, the process is liable to be 
deficient in structure. 

This deficiency in structure is easily demonstrable, in persons 
of middle age or of later life who have had teeth extracted, and 
a part of the alveolar process has come away. By frequent ob- 
servation it will be seen that the process is not restored although 
the periosteum is still present. Again after the extraction of a 
tooth, although the alveolar process remains normal about the 
adjoining teeth, a slight absorption of the edges of the alveolus 
about the cavity will take place. The gums heal over the wound. 
By the use of a broken excavator, sharpened in a direct line with 


the shaft at the point, this may be readily passed through the 
soft fibrous tissue of the once root cavity. Years after the ex- 
traction, fibrous tissue without lime salts, is present. The same 
is true when abscesses have formed. The fibrous tissue is re- 
stored but not the bone substance. Regulating teeth should be 
performed before the patient has obtained his growth and with 
as little movement of the teeth as possible to obtain fairly good 
results. The indiscriminate spreading of the dental arch with- 
out extraction should be discouraged. The excessive inflamma- 
tion set up throughout the entire alveolar process for the pur- 
pose of enlarging the dental arch and thus bringing all teeth into 
line is liable to endanger the restorative process. 

I have a record of forty-two patients in whom the teeth re- 
mained loose from a want of deposition of bone cells to hold them 
in position and in whom the roots of the teeth were exposed to 
a greater or lesser extent. Interstitial gingivitis is always pres- 
ent and occasionally pyorrhoea alveolaris. The esthetic effect 
of the large dental arches associated with a small face is not in 
harmony with good judgment. 

The nerve strain, the inartistic appearance and excessive in- 
flammation should be reduced to a minimum by adopting such 
measures as are necessary to perform the operation as quickly as 
possible with as little nerve strain and with the least amount of 
work, to avoid interstitial gingivitis. 

The removal of bone in front of the advancing tooth or teeth 
with a burr (as I have recommended) will save time, prevent 
undue inflammation, pain, nerve strain, and absorption. 


Plantation of teeth consists of two methods. One the re- 
placing of a tooth into the cavity from which it has been acci- 
dentally removed or a similar tooth has been taken from the 
mouth of another person, while the other is the insertion of a 
foreign tooth either into an enlarged natural socket or into an 

6 A young woman nineteen years of age called at my office for advice in regard 
to the restoration of the alveolar process about the six anterior inferior teeth. 
The bone had Keen destroyed in regulating. Retaining bands had been in place 
about two years. The operator was afraid to remove the bands for fear that 
the teeth would drop out. It was impossible to restore the process. 


artificial alveolus which has been made for its reception. The 
replantation of a tooth which has been forcibly removed in a 
healthy growing child in most cases, if skillfully performed 
under aseptic conditions, will return to a normal condition with- 
out chronic inflammation. 

On the other hand, from what we have learned from the un- 
stable nature of the alveolar process and the many difficulties 
associated therewith, we hardly expect many favorable results 
by the enlargement of natural sockets or the formation of new 
sockets. By these operations the peridental membrane is de- 
stroyed in the one case and not present in the other. Interstitial 
gingivitis, with lacunar absorption of the root (which is a foreign 
body) takes place or absorption of the alveolar process by 
halisteresis ensues or both with the eventual loss of the tooth. 

If the patient has obtained his growth, the chances of success 
are hardly to be expected. Especially is this true if the patient 
has autointoxication or other poisons in the blood or is subject 
to disease of any of the eliminating organs. 

There are many other irritants, both constitutional and local, 
not mentioned by the author. Enough have been cited, however, 
to give the reader a fair idea of the influence of these irritants 
upon the alveolar process. 

When inflammation is once established in the gums or alve- 
olar process by local or constitutional conditions, it is usually 
progressive as far as the exfoliation of the tooth. If, however, 
the inflammation is circumscribed and does not extend entirely 
around a tooth which has one root, or, if only one root of a molar 
is involved, the inflammatory process, with absorption will have 
a limited area and extend only on one side of a single root or 
may involve only the one root of a molar tooth. This inflamma- 
tion and absorption will progress to the end of the root. In other 
words, the disease is progressive after it has become established 
although treatment both local and constitutional may to a certain 
limit retard its progress. Illustrations of this may be recalled 
in those teeth which have been violently wedged apart to obtain 
room for filling and the inflammation extends along one side of 
a tooth, or, when gold crowns have been carried under the gums 


and irritation has set np uniformly around the tooth, or, in teeth 
which have too much pressure in mastication, or, in those teeth 
for which there are no opposing teeth. The progressive nature 
of inflammation and absorption is due to the endo-transitory 
nature of the process. 



Pathological changes in the structure and function of the 
human body, in a more or less severe form, are due to constitu- 
tional affections. Sometimes they are the result of local diseases 
of certain organs, or the disease may have general character- 
istics from the first and still may affect certain individual organs, 
hence in this way secondary diseases are developed. This has 
been particularly borne out in trauma, intoxications, contagious 
infections and some tumor-like forms. 

Diseases are designated as acute and chronic. Acute dis- 
eases are those of short duration. The acute stage may be ter- 
minated promptly in recovery or death or it may be prolonged in 
the chronic period. Disease may occur with or without reducing 
the tonicity of the body as a whole or a part. 

Fever is a general metabolic disturbance, characteristic of 
many acute infections and autointoxications. The most impor- 
tant indication is a rise in the temperature of the body. The su- 
perficial temperature of a man normally varies considerably but 
the internal degree of heat is nearly constant. According to the 
researches of Jurgensen, Ziemssen and Krabler 1 the minimum 
internal degree of heat is during the early morning hours and 
the maximum is reached at about five o 'clock in the afternoon. 

In pyrexia, along with an increased production of heat, there 
is also an increase of nitrogenous metabolic products excreted 
in the urine. In regard to heat the amount thrown off varies; 
thus in the early stages of fever when the internal temperature 
is increasing, the surface temperature is below normal with con- 
tracted vessels and the amount of heat dissipation is lessened. 
Since the skin produces but a small amount of heat, its warmth 
is dependent upon the heat brought from the interior of the body, 

iThoma, Text-Book of General PathoWv. 


so if the skin vessels contract, the amount of blood that flows to 
the surface is lessened and the temperature of the skin falls. 

The lessened amount of heat thrown off together with the 
greater production causes a rise within the body, although aside 
from a slight feeling of cold, there may be no apparent change 
in temperature. But if there is marked contraction of the skin 
vessels, the chilliness is more pronounced, so much that there 
may be violent shivering of the trunk, limbs and chattering of 
the teeth. The violent contraction of the skin muscles produces 
heat. When the fever is at its highest, the contracted cutaneous 
vessels yield, the skin becomes abnormally dry and hot, while 
the internal temperature remains high also. When the fever sub- 
sides, the temperature falls and the skin becomes moist, or there 
may be an excessive amount of sweat. 

Other symptoms of pyrexia aside from temperature rise are 
malaise, headache, thirst, rapid pulse and respiration, digestive 
disturbance and decrease in the amount of urine secreted and 
passed with abnormal urinary acidity and oftentimes indican. 
In digestive disturbance, primarily, there is loss of appetite, ex- 
cessive thirst, the salivary secretions are restricted and the 
entire alimentary tract becomes so affected as to prevent normal 
al (sorption from the stomach and intestine. The digestive and 
metabolic disturbance may be less than is usually assumed. Ex- 
periments show that in typhoid the digestion, absorption and 
utilization of food may be complete. 

In a search for the connecting etiology of these fever symp- 
toms we must first take into consideration the infections and in- 
toxications from which they are derived. Disease producing 
germs, by their poisons when they enter the blood, cause fever. 
It may be that many substances produced by the metabolism of 
the human body have similar action. There are also poisonous 
agents not derived from microbes which cause temperature rise. 

Fever appears to consist of two sets of symptoms, toxemia 
and pyrexia. The first are due to the direct action on the nervous 
system while the second constitute a reaction on the part of the 
system which tends at least to neutralize the effects of the tox- 
emia. According to the researches of Vaughn, the poisonous 
substance is a derivative of the albumin molecule resulting from 


a splitting such as occurs in digestion or in the destruction of 
bacteria by the blood serum (bacteriolysis). Thus certain veg- 
etable proteins, like recin, peptones, and the results of the split- 
ting of bacterial proteins excite fever. Metallic and alkaloidal 
poisons do not, as a rule, cause fever except by provoking in- 
flammation which results in secondary bacterial infection. When 
these poisons are taken into the blood stream, a general faulty 
metabolism results which gives rise to the symptoms just men- 
tioned. In regard to the pyrexia} rise of temperature, partic- 
ularly, it must be conceded that the poisons circulating in the 
blood have a disturbing influence on the structures of the cen- 
tral nervous system as well as on the vasomotor system of the 
peripheral nerves. The loss of heat, through the breath, is also 
controlled by the central nervous system which acts on the fre- 
quency and depth of respiration. 

The normal heat of the body is produced by every organ in 
its metabolism. The principal heat producing sources, however, 
are the heart, muscles and principal abdominal organs. The 
energy of the heart muscle, when it contracts is exhibited partly 
as heat and partly as mechanical work. The heat produced by 
the contraction of the heart is partly radiated into the surround- 
ing tissues and partly carried away by the blood. In addition, 
the mechanical work of the heart is completely transformed into 
heat by friction against the vessel walls and internal friction 
within the blood stream. The muscles all generate heat by their 
action. The disturbance of assimilation, digestion and absorp- 
tion of food occurs at the same time, during fever, with temper- 
ature rise. This in turn causes metabolic disturbances not only 
of abnormal products but also a breaking down of organic cells. 
This may occur in various organs and there may appear any of 
the cerebral disturbances, such as headache, confusions, dizzi- 
ness ; also rapid decay of the teeth, interstitial gingivitis ; ab- 
sorption of the alveolar process ; diseases and spontaneous death 
of the pulps of the teeth; erosion; abrasion and discoloration. 
After fevers, loss of the hair and abnormalities in the nails usu- 
ally make their appearance. 

Degeneration of tissues which form the substance of the 
heart, liver, kidneys and other structures, are partly due to dis- 


turbances of high pressure and partly due to the direct action 
of poisons circulating in the blood which have caused the fever. 
It would not be strange, therefore, that similar degenerations 
occur as a result of simple action of poisons in non-febrile acute 
diseases as well as in poisoning by the various inorganic and 
organic chemical substances. 

Chronic diseases are those of long standing and are usually 
the result of a prolonged acute condition. Generally there is no 
rise of temperature though there are instances of pyrexial and 
apyrexial periods alternating. 

In a general way, I have explained the cause of some chronic 
diseases, contagions, infections and intoxications, but there are 
some constitutional disorders, for example, chlorosis, leukaemia, 
rachitis, obesity, gout, diabetes, osteomalacia whose etiology is 
still vague, yet are manifested by disturbed metabolism. Path- 
ologic conditions to which these diseases give rise are many but 
the two most common are atrophy and malnutrition. One of 
the best examples of atrophy in the human body is the alveolar 
process. Atrophy as applied to the tissues and organs of the 
body is somewhat different in its action on the alveolar process. 
In all the other tissues and organs, atrophy means a gradual 
wasting away of structure. While the same condition takes place 
in the alveolar process, in addition to the wasting away, there is 
total destruction, owing to the fact that the process is a doubly 
transitory structure and an end organ. In the mouths of the con- 
genital deaf, dumb, blind, feeble-minded and delinquent chil- 
dren, osteomalacia attacks the alveolar process before the 
osseous system has reached its growth. Here, as a consequence 
of trophic change, metabolic action and premature senility, 
osteomalacia may occur in connection with the first set of teeth 
at two years or any period thereafter. When this condition 
takes place early in life, I have called it "juvenile osteomalacia," 
late in life ' ' senile. ' ' - 

It is those organs of special function which become diseased 
and atrophy to the greatest extent ; thus in the liver, the cell ; in 
the kidney, the secreting epithelial cells; in the heart, the muscle 
fibers; in the spleen, the pulp cells; in the subcutaneous tissue, 

2 Pathogeny of Osteomalacia or Senile Atrophy. The Dental Digest, August, 1903. 


the fat cells; in the lungs, the stroma of connective tissue and 
elastic fibers, the blood vessels and epithelial lining ; in the bones, 
including the alveolar process, the lamella?; the skin becomes 
thin and loses its tonicity ; the epidermis dry, cracked and scaly ; 
the brain diminishes and the space is filled either by atrophy of 
the skull or fluid in the pia-arachnoid. 

Cachexia is characteristic of organ degeneration of a chronic 
type. In this condition, amyloid degeneration is sometimes as- 
sociated with albuminous and fatty degeneration of the liver, 
kidney, heart muscle, etc. The fatty tissue is lost. The epi- 
dermis, unlike the marasmic states, is smooth and moist. The 
blood composition becomes changed, in many instances producing 
capillary hemorrhage or edema. Then, too, the weight of the 
body and organs is reduced, showing that cachetic conditions 
are a general disturbance of metabolism. Aside from its chronic 
character and absence of temperature variability, there are 
many similar features to those of the pyrexial disturbances of 


Having considered the more severe constitutional disturb- 
ances in which fever is always present, we must now briefly con- 
sider those constitutional disturbances so fatal to the alveolar 
process and in which fever does not manifest itself. 

One of the most common causes of irritation producing in- 
flammation and absorption of the alveolar process is the acid 
condition of the system. In the human body certain changes are 
continually taking place. These changes take place in the fluids 
of the body and are both physiologic and chemic. These changes 
add to and take away tissues of the body and are alkaline or acid. 
They are called anabolic when the fluids are alkaline and the tis- 
sues are built up and katabolic when the fluids are acid and the 
tissues are broken down. The alkaline and acid states of the 
body may be ascertained by the examination of the excretions 
of the body. When the fluids of the body (except the gastric 
juice) have an excess of acids the saliva, mucus, perspiration 
and urine will be excessively acid. When the secretions of the 


body are acid it indicates that there is a diminished alkalinity 
of the blood. This in turn leads to improper functioning and 
prevents proper nutrition and produces lowered vitality. 

It is known that an acid excess in the system will hinder and 
often destroy the transmission of nerve impulses. Thus in acid 
states large areas of skin will be without sensation; the knee 
jerk is diminished or lost altogether. A continued acid condi- 
tion of the system will cause nerve end degeneration in the pulps 
and fibrillar of the teeth. The teeth will discolor, become brittle 
and the enamel and dentine will break off. In no part of the 
body does the excessive acidity manifest itself as in the alveolar 
process. Its endo-transitory nature makes it very susceptible to 
irritation through its nerve filaments and its end arteries, set- 
ting up irritation and inflammation. When the fluids of the 
body are acid the alveolar process and mucus excreted are, 
therefore, acid to a greater or less extent, nutrition is thus cut 
off and absorption of the process takes place. Thus in acid 
states, as well as in dental states, the alveolar process gradually 
absorbs away. 

In dealing with the influence of buccal states on the constitu- 
tion it must be remembered that when the eliminatory system is 
overstrained, especially when the poison-destroying function of 
the liver is deficient or impotent, the alveolar process and gums 
play a great part in elimination, whence come, for example, the 
"blue" gums of lead poisoning and the "green" gums of brass, 
as well as those from mercury, arsenic, potassium iodid, bromid, 
etc. Matter thus eliminated is reabsorbed, enters into the chyle 
with digested products, and readily becomes toxic to the blood 
cells. That cachetic states, approximating pernicious- anaemia, 
can thus be produced, is clearly evident. Were fecal anasmia 
existent before the gum and alveolar process changes were set up 
it would thus be greatly intensified. The toxemia producing this 
gum and alveolar process state would be greatly increased 
through the overstrain of oxidizing processes produced by re- 
absorption of eliminated products. 

The toxins generated in the mouth readily pass into the gen- 
eral system. As a result, chronic indigestion with coexistent 
pigment spots, urticaria, etc., may occur. Pus toxins may thus 


produce a sapremia mimicing typhoid, as pigment spots readily 
simulate the typhoid eruption. In buccal manifestations of con- 
stitutional disease the vicious circle of pathology peculiarly 

The alveolar process may be affected at any period of life 
after the eruption of the first set of teeth but osteomalacia does 
not usually occur until the period between twenty-five and thir- 
ty-five. Before this the osseous system is in its constructive 
state and lime salts are being deposited rapidly. Later in life 
the constructive stage is complete and material sufficient only 
to repair waste is deposited. At the periods of stress metabolic 
changes are most active — during puberty and adolescence (four- 
teen to twenty-five), during the climacteric (forty to sixty), 
when uterine involution in women and prostatic involution in 
men occur and finally during senility (from sixty upwards), 
when the disease is always present to a greater or lesser degree. 
While in allied conditions men are most influenced, in this dis- 
order the sexes seem to be affected about equally. Here the in- 
fluence of pregnancy comes into play. Pregnancy disturbs the 
physiologic balance hitherto existing, especially along the line of 
assimilation and elimination. The well known dental effects of 
pregnancy (whose underlying cause affects the alveolar proc- 
ess) are due to this factor. This is purely a constitutional 

Among the causes are non-elimination of toxic substances, 
whether due to autointoxication, to bacterial action, or to me- 
tallic and vegetable drugs. Disorder or disease of any excretory 
organ (kidneys, bowels, skin or lungs) will produce the most 
marked effect, first upon the constitution of the blood, and second 
upon the alveolar process, with resultant osteomalacia. 

The urine, as has been shown, contains each day in a normal 
individual sufficient toxins to cause death if not excreted. This 
condition is markedly increased after prolonged nervous ex- 
plosions like those of epilepsy or hysteria. This was pointed 
out thirty years ago by Meynert, who demonstrated that the 
status epilepticus (condition of rapidly-recurring convulsions) 
was due to the accumulations of a proteid body in the system. 
The status epilepticus is preceded by a decrease of toxins in the 


urine and succeeded by an increase. This is likewise true as to 
the influence of non-elimination by the other excretory organs 
(bowels, lungs and oral cavity), as well as to the non-exercise 
of its poison-destroying power by the liver. Non-elimination 
moreover interferes with ordinary digestive functions and 
hence increases its own extent. Another factor in autointoxica- 
tion is production of toxic products in such quantity as to pre- 
vent destruction by organs like the liver and consequent elim- 
ination, since a product to be properly eliminated must be 
changed to a particular chemical type. Among the factors 
which affect both these elements of elimination is the power 
over growth and repair exercised by the nervous system. In 
part this influence is exerted through control of blood supply by 
the vasomotor nervous system, and in part by that direct con- 
trol of the nervous system over tissue change which is known 
as its trophic function. 

Both influences are affected by nerve strain. Sudden emo- 
tion may, as Bichat demonstrated decades ago, produce marked 
defects upon bile secretion and may occasion jaundice. Cases 
are far from infrequent in which emotions like jealousy pro- 
duce a mimicry of gall-stone colic in neuropaths. Murchison, 
Christison and Thompson have traced attacks of biliary colic 
to jealousy. Other liver changes from sudden nervous disturb- 
ance, whether of mental type or not, are not rare. As mental 
impressions are communicated to the central nervous system 
purely through mechanical changes in the nerves, such influence 
must be purely material in operation. As the brain exercises a 
checking influence on the operations of the liver, these mental 
influences produce two effects. The mental shock increases the 
checking action of the central nervous system on the local 
ganglia of the liver, and destroys the checking action of the liver 
ganglia, and in consequence these go too fast, resulting in their 
exhaustion. Either of these conditions interferes with the 
poison-destroying action of the liver, and accumulation of waste 
products is the result. 

What is true of the liver is true of the other organs. This 
is especially noticeable, as Tuke points out, in regard to the 
kidneys. The action of mental anxiety or suspense, in causing a 


copious discharge of pale fluid, is familiar enough to all, espe- 
cially to the medical student about to present himself for exam- 
ination, the amount being in a pretty direct ratio to his fear of 
being plucked. The frequency of micturition may, however, 
arise from nervous irritability of the bladder without increase 
or even with diminished secretion. Still the action of the skin is 
usually checked, the extremities are cold, and the kidneys have 
to pump off the extra amount of fluid retained in the circulation. 
Elimination of the substance usually separated from the blood 
is diminished as compared with the aqueous character of the 
whole secretion. The odor may be affected by the emotions in 
man as in animals. Prout is of the opinion that mental anxiety 
will produce not only non-elimination but also change in the 
chemical character, as indicated by odor and otherwise. Disturb- 
ances in the medulla produce, as Claude Bernard long ago 
showed, a markedly pale, excessive urine. These disturbances 
often arise from intellectual strain or emotional shock. The in- 
fluence of emotional states on secreting processes, and thereby 
indirectly upon autointoxication states, is illustrated in the fact 
long ago pointed out by Tuke that pleasurable emotions increase 
the amount of gastric juices secreted, the opposite effect being- 
produced by depressing passions. Beaumont found in a case of 
gastric fistula that anger or other severe emotions caused the 
gastric inner or mucous coat to become morbidly red, dry and 
irritable, occasioning at the same time a temporary fit of 

The influence of fear and anxiety on the bowels is as well 
marked as that upon the bladder and kidneys. Apart from mus- 
cular action, defecation may become urgent or occur involun- 
tarily from various causes. The increased secretion from the 
intestinal canal may occur from fear and in some cases from the 
altered character of the secretion itself. While in this respect 
the influence of fear may be inconvenient in man, it naturally 
assists escape in some animals, as the skunk. 

Emotions powerfully excite, modify or altogether suspend, as 
Tuke has shown, the organic functions. This influence is trans- 
mitted not only through the vasomotor nerves but through 
nerves in close relation to nutrition and secretion. When the 


excitement is of peripheral origin in sensory or afferent nerves, 
it excites their function hy reflex action, so that as emotion arises 
it may excite the central nuclei of such afferent nerves, and this 
stimulus be reflected upon the efferent nerves, or it may act di- 
rectly through the latter. Pleasurable emotions tend to excite 
the processes of nutrition, hence the excitement of certain feel- 
ings may, if definitely directed, restore healthy action to an af- 
fected part. Violent emotions modify nutrition. Various forms 
of disease originating in perverted or defective nutrition may 
be caused primarily by emotional disturbance. Emotions, by 
causing a larger amount of blood to be transmitted to a gland, 
increase sensibility and warmth and stimulate its function or 
directly excite the process by their influence or nerves supplying 
the glands. Painful emotions may modify the quality (i. e. 
the relative proportion of the constituents) of the secretions. 

Imperfect elimination of effete matter from the lungs is a 
fruitful source of autointoxication. The more marked forms are 
those of tuberculosis, in which there is great debility and in 
which there is greater waste than repair. Self-poisoning is con- 
tinually going on and will continue until death. The chest 
capacity for the inhalation of pure air is almost nil, hence the 
blood is improperly oxygenated and soon ceases to convey 
nutriment to the tissues. Eight per cent of criminals who die 
of tuberculosis in prisons have undeveloped chest walls. De- 
generacy therefore cuts quite a figure in the role of autointoxi- 
cation. Degenerates with contracted chest walls are, however, 
more frequently found. Many undeveloped individuals in every 
walk of life for this reason have tuberculosis. People with un- 
developed chest walls and chest capacity may not have tuber- 
culosis and yet may suffer from autointoxication. Those who 
have had pneumonia with adhesion; and who are thus unable 
to oxygenate the blood, are subject to this disease. Asthmatics 
and hay-fever patients suffer from autointoxication and alveolar 
absorption. When the skin is overstrained as to excretion 
through kidney and bowel overstrain, the lungs are forced to 
take on increased work with imperfect oxygenation as a result. 
This is noticed in the odor of the breath in Bright 's disease and 
in the air-hunger of diabetes, etc. In nerve-strain states and 


in the condition described, by Albu not only do excretory organs 
suffer but the secretions of those glands like salivary and buc- 
cal glands are so altered as to become irritants. These ex- 
cretory conditions not only result upon autointoxication states 
but are modified by trophic nerve function alterations. By 
trophic changes are meant such tissue alterations as occur in 
morbid conditions from disordered function of the centers of 
nutrition. Peripheral as well as central may be involved. The 
well known law of Wallerian degeneration of nerve fibers is an 
illustration, the posterior ganglion acting as a trophic center 
for the fibers of the posterior root in the cord itself. Trophic 
action may therefore be peripheral, though in extensive changes 
as a rule central (cerebral or spinal) origin should be looked 

The constitutional result of acute and chronic infection and 
contagions is apt to be an autointoxication plus the action of 
the germ toxin. All the exanthemata have at times been fol- 
lowed by wasting or necrosis of the alveolus. Here the con- 
dition is notably symmetric and accompanied by disorders of 
the osseous system elsewhere. The same is true of grippe and 
tuberculosis. The well-marked disorder known as Eiggs' dis- 
ease has been charged by Pierce, Kirk, Ehein, Eobin and Magi- 
tot to the direct influence of an arthritic state (gouty and rheu- 
matic) and regarded as a special type of arthritic manifestation. 
The alveolus is clearly vulnerable to the toxins of many infec- 
tions. It is likewise quickly affected by some autotoxic influ- 
ences from disordered metabolism. Its vital resistance to these 
agencies is less than that of other tissues. It is the earliest 
sacrifice when these or any toxins disturb the harmony of the 

A cause other than the actions of toxins exists for impli- 
cation of these parts. Whenever tissue waste, whether local or 
general, exceeds repair there is trophic change. This latter 
depends directly upon disordered local or general nervous func- 
tions. Trophic alterations from the first cause appear in growth 
disorders of the nails and loss of hair (alopecia) after fevers, 
the most familiar obvious examples of this pathologic process. 
Of the other type are localized atrophies where the direct inter- 



vention of toxins can be excluded. The alveolus is liable to the 
first form of trophic deterioration. The influence of acute dis- 
eases upon the alveolus is probably thus exerted in many cases 
rather than by direct infection. Where no cause has been as- 
certained examination directed to this factor would probably 
reveal it. The general failure of the trophic centers after the 
prime of life (in senile states), which is attended with loss of 
teeth and wasting of the alveoli, is the most obvious instance 
of trophic failure affecting the part. Even simple anaemia may 
thus give rise to alveolar wasting. 

Another constitutional disorder in which the alveolus is 
early affected is diabetes. The exact pathology of this is un- 

Fig. 75. — Absorption by Halisteresis. Three Small Arteries are Seen. Two 
in the Upper Part of the Illustration with Round Cell Inflammation Just 
Beginning, while Another Small Artery is Located at the Lower Border 
of the Large Absorbed Area. 

certain, but in many cases at least it is largely dependent on 
disordered action of the central nerve system. Renal disease 
is another common condition which tests the vulnerability of the 
alveoli. An ideally normal kidney is probably rare, but only 
when its abnormalities pass beyond a certain point can it be 
called diseased. In the less advanced conditions that have 
passed the line of morbidity, alveolar implication is often very 


marked. This may be one cause of the unusual frequency in 
the insane, who are especially liable (as Bondurant and others 
have shown) to suffer from renal disease. They are very liable 
likewise to autointoxications and trophic disorders as well, 
since the balance of the nervous system has been upset. Some 
(the paretic and organic dements) exhibit especial tendencies 
to trophoneurotic disturbances affecting the teeth. In states of 
depression and stupor, circulatory disturbances predispose to 

The constitutional results of acute and chronic infections 
are apt to include autointoxication in addition to the action of 
the toxins of their germs. The eruptive fevers, especially 
scarlatina or measles, have been long known to be followed by 
wasting or necrosis of the alveoli. Here the condition is notably 
symmetrical and unaccompanied by exfoliation or necrosis of 
the osseous system elsewhere. Tuberculosis does not spare 
the alveolar process. 

The more marked forms of constitutional disorders (typhoid 
fever, pneumonia, tuberculosis, syphilis, indigestion and preg- 
nancy, etc.) produce intense results. 

The second form of trophic failure in the alveolus is less 
prominent, since it generally coexists with overshadowing dis- 
turbance elsewhere which it creates to a certain extent. Cruvei- 
lier noticed its occurrence associated with simple paraplegia, 
regarding it as of nervous causation. In facial hemiatrophy 
local wasting of the alveolus has appeared before the disorder 
has involved the jaws generally. This is sometimes due to a 
local cause, but its occurrence and association with other neuro- 
trophic symptoms are suggestive. 

We have seen that the action of the heart plays quite a role 
in the constitutional diseases of the body. Constitutional dis- 
eases affecting the heart and diseases of the heart itself cause 
excessive and diminished action of this organ. This excessive 
and diminished action causes changes in the flow of the blood 
in the peripheral capillaries. Those organs first involved in 
this change of heart pressure are the end organs of the body. 
The alveolar process, therefore, being the most sensitive end 



organ, because of its transitory nature and its bony substance 
is one of the first to be involved in autointoxication. 

In intestinal putrefaction, hepatic and renal insufficiency and 
drug poisoning as well as in other diseases, the heart becomes 
enlarged and a high blood pressure is developed. Dilation of 
the arteries occurs, especially in those of end organs, resulting 
in arterio-sclerosis, which is present in every case. 

; . — Shows Bone Absorption by Halisteresis 
Canal Absorption. 

and Volkman 

To ascertain the blood pressure in patients suffering with 
interstitial gingivitis I used Cook's modification of the Eiva 
Rocci sphygmomanometer, this instrument being best adapted 
for my convenience and exceedingly simple. The armlet used 
was sold with the instrument and consists of a rubber bag 4% hy 
40 cm. The patients ranged from twenty-seven to sixty-seven 
years of age. With this instrument the normal adult female 
arterial blood pressure is 115 to 125 mm.; adult male, 125 to 
135 mm. 

In twenty-six females there were three who ranged between 
115 mm. Hg. and 125 mm. Hg. and therefore normal. Three 



ranged below 115 mm. Hg., and twenty from 133 mm. Hg. to 
180 mm. Hg. 

In twenty-four males there were eight who ranged between 
125 mm. Hg. and 135 mm. Hg. and therefore normal. Three 
ranged below 125 mm. Hg., and thirteen from 133 mm. Hg. and 
160 mm. Hg. 

When we consider that thirteen of these patients were un- 
der forty-five years of age, the high blood pressure is remark- 

I have been unable to demonstrate whether the interstitial 
gingivitis is accelerated directly because of the poisons circulat- 

, **4*' 

[• ;t -V *-y 


-Illustrates Lacunae oh Osteoclast Absorption. 

ing in the blood vessels, causing high blood pressure by their 
action upon the heart, or because of their action upon the vaso- 
motor nerve governing the heart or blood vessels, or both. The 
effect of the toxins and extra blood pressure is to set up irrita- 
tion and inflammation of the outer surfaces of the Haversian 
canals, producing halisteresis in the vessels of Von Ebner, pro- 
ducing Volkmanns ' perforating canal absorption and setting the 
osteoclasts at work, all producing absorption of the alveolar 



The question arises, which end organ is the most susceptible 
and first involved in autointoxication? When a man visits 
the physician for treatment one of the first questions asked is, 
"What is your occupation?" If the man replies that he is 
working in drugs, metals or mines, the physician examines his 
patient's gums to note if his system be saturated with poisons. 
If a physician is treating a patient for lues, the drug is adminis- 
tered until the "gums are touched," which is the only indica- 
tion his patient is under the influence. One of the most marked 
symptoms of scurvy is the inflammatory condition of the gums 
and alveolar process, which are always taken into consideration 
in diagnosis. 

Fig. 78. — Lower Portion Showing Absorption* op the Alveolar Process 
Below the Roots of the Teeth. 

Physicians agree that the arteries in such end organs as the 
kidneys, brain and retina dilate under blood pressure. The 
arteries ramifying bone structure, dilate only imperfectly, if 
at all. Arteries entering transitory bone structures gradually 
undergo pathologic changes. After the individual has obtained 
his growth these arteries certainly are more susceptible to toxin, 
poison and blood pressure than those in the kidney, brain 
or retina. I have demonstrated these pathologic changes in 
the alveolar process many times. The toxic products circulat- 
ing in the blood affect the heart and cause a high blood pressure. 


High blood pressure, together with toxic products circulating 
in the blood, set up inflammation in the alveolar process and 
gingival border. In the alveolar process, first, because the ar- 
teries in the soft gum tissues, under high blood pressure, can 
and do expand and the tissues recover as soon as the cause is 
removed, but the arteries running tortuously through the bone 
cannot expand to any appreciable extent, and the blood pressure 
and toxic products cause inflammation and absorption of bone 
tissue without restoration. Hence the term "interstitial gin- 
givitis" (deep-seated inflammation in the alveolar process). 
Cardio vascular, nervous, hepatic and renal diseases, as re- 
lated to interstitial gingivitis, are therefore due to the same 
cause. In relieving or removing the cause of interstitial gin- 
givitis the other symptoms and diseases are relieved, and vice 

Figure 75 illustrates a large area of absorption with destruc- 
tion of the fibrous tissue to a larger extent. Around the border 
is seen a small amount of inflamed fibrous tissue. An artery, 
once an Haversian canal, is also seen. About the large area 
are also seen three Haversian canals with the inflammatory pro- 
cess just beginning. 

Figure 76 shows four centers of absorption at Haversian 
canals. Through the picture may be seen dark lines running in 
all directions. These are vessels of Von Ebner, through which 
Volkmann's canal absorption takes place. A beautiful illus- 
tration of this is the canal running from one large area of 
absorption to the other. 

Figure 77 shows the third form of bone absorption — lacunae 
or osteoclast absorption. Here a large area of bone is destroyed 
by these large cells. 

Figure 78 is a low power, showing the distribution of the 
alveolar process between the roots of two teeth. Very little 
of the bone remains. When the trabecules or fibrous tissue is 
destroyed in large areas, and especially in transitory struc- 
tures, it is rarely restored. 



One of the simplest forms of constitutional disturbances 
which produce interstitial gingivitis is that of climatic changes. 
The effect of climate which includes heat, cold, moisture, dryness 
is generally recognized by physicians as having much to do with 
the action of disease upon the system. To such an extent has 
this subject been impressed on the profession that the late Dr. 
N. S. Davis of Chicago, many years ago organized a separate 
section in the American Medical Association on Climatology, 
while every medical congress has its section on Tropical Medi- 
cine. If this subject is of so much importance in the cause and 
treatment of disease, especially in its influences upon the ex- 
cretory organs, how much more important must it be in relation 
to interstitial gingivitis, since the alveolar process, being a 
doubly transitory structure and an end organ, is always the 
first affected by sudden and prolonged changes. 

Experiments have shown that cold acts as a stimulant and 
increases the amount of carbonic acid exhaled, while experiments 
made by Dfluger and Marcet also show that a similar increase 
from heat would produce the same result. Both cold and heat 
then to a certain point act as stimulants. 

The judicious change in climate, that is, moving in winter to 
warmer climates and vice versa, taking into consideration mois- 
ture, light, rarification or condensation of air and the increase 
by the variations in the manner of life and hygiene may prove 
beneficial or disastrous according as the organs respond to the 
changed environment. 

In low temperature, the body loses more heat and the loss 
must be supplied. The older the individual the more marked 
is the effect of excessive cold and heat. The effects upon the 
individual are the same as in high temperatures, in part through 
local injury and death of tissue, in part through refrigeration 
of the entire body. Severe and lasting lowering of tempera- 



ture causes tissue death; after mild chilling has occurred, as 
the result of tissue degeneration, thrombosis, hyperaemia and 
exudations which are relatively rich in leucocytes. A very short 
refrigeration at the freezing point is sufficient to produce de- 
generative changes which are quickly followed by regenerative 
proliferation on the part of the cells remaining uninjured. Tips 
of the extremities, nose, ears, fingers, feet and toes, are the most 
easily frozen because of their extreme distance from the heart. 

According to Ziegler, "Besides the more severe forms of 
local or general lowering of the tissue temperature there may 
occur, as harmful pathogenic influences, mild, general or local 
chillings, the so-called colds, as the result of which disease- 
phenomena may manifest themselves partly at the seat of chill- 
ing, partly in organs in distant parts of the body. For example, 
after widespread refrigeration of the skin there may occur 
diarrhoea, catarrh of the respiratory tract, or disease of the 
kidneys; after local chilling of the skin, painful affections of 
the deep-seated muscles. The exact relation between these phe- 
nomena and the refrigeration is unknown (the oft repeated 
hypothesis that they are due to hyperaemia of the internal or- 
gans caused by the chilling of the body surface has not been 
proven), but there is no reason on this account to deny the exis- 
tence of diseases caused by cold. Though many diseases for- 
merly attributed to "catching cold" have been known to be 
of infectious origin, there yet remain a number of diseased con- 
ditions for which we know no other etiology than that of 
refrigeration. Conditions of the body in which the skin is hy- 
peraemic and the perspiratory function active favor the taking 
of cold. Many individuals appear to possess a predisposition 
on the part of certain tissues to the effects of refrigeration; in 
one person certain muscles, in another the mucous membranes 
will be affected. 

According to the view of many writers, refrigeration of the 
body increases the susceptibility to infection, so that, for ex- 
ample, the pathogenic bacteria which may be present in those 
cavities of the body accessible from without, may, after such 
refrigeration, be able to exert their injurious influences upon 
the tissues." 


There is a great difference between radiated or sun heat and 
shade heat. Sunstroke is rare in the pure and comparatively 
dry air of high elevation. The same is true on the ocean. Shade 
heat, on the other hand, can be borne less easily. One can do 
hard work in the sun heat when one would rapidly become ex- 
hausted in shade heat at one-third the temperature. People 
bear heat very differently. The manner of living must neces- 
sarily be taken into consideration. It has been shown that Eu- 
ropeans who go to live in hot climates are injured by continuing 
the same kind and amount of food and stimulants as they are 
accustomed to use at home. Parkes says, "great heat in shade 
exerts a depressing influence lessening the great functions of 
digestion, respiration, sanguinifieation and directly or indirectly 
the formation and destruction of tissue." 

Dr. Gr. D. Boak states as to Philippine climatic effects upon 
the teeth: "While the weather is by no means as hot as it is 
at times during the summer in the States, the average tempera- 
ture for the islands is about 89° F. It is a continuous heat with- 
out invigorating change of seasons. This gradually saps vital- 
ity and enervates, producing the lassitude which is characteris- 
tic of the tropics. Enervation produces anaemia, with corre- 
sponding lessening of the resisting powers from the lower 
vitality, especially in those who have lived previously in tem- 
perate climates. Caries is frequent and progresses rapidly 
in this climate." This Dr. Boak attributes to the following 
causes : First, lowering of the vitality by a lessening of the 
resisting powers ; second, acidity of the oral secretions. 

Among important factors to be considered in connection with 
hygiene in the tropics are the questions of dietetics as well as 
the effects of moist and dry heat. The two last produce, as 
elsewhere shown, a neurasthenia with co-existing and complicat- 
ing autointoxication. These two peculiarly affect the alveolar 
process. It is, therefore, not remarkable to find in a recent 
report by General Otis, the case of Walter Fitzgerald, Com- 
pany C, twenty-ninth infantry, formerly of the Montana volun- 
teers, cited. This twenty-three-year-old man had been in the 
Philippines for a year and seven months. He was one of the 
first volunteers to reach Manila after the naval battle. Nine- 


teen months' life in the tropics on the usnal army rations had 
resulted in the loss of nearly every tooth. While the climate 
undermines nutrition of the alveolar process, and tropical fevers 
have the same effect, improper diet increases the defect. In the 
case of Fitzgerald, the teeth dropped out one by one, as is com- 
monly the case with Americans in the Philippines. 

Soldiers going from a temperate climate to Cuba and the 
Philippines with change of food, had autointoxication and in- 
terstitial gingivitis. 

In an examination of the soldiers and officers of two com- 
panies who had just returned from the Philippines, located at 
Fort Sheridan, Illinois, I obtained the following results : The 
total number examined was 127. American, 98; 'Irish, 12; 
German, 9; English, 3; Norwegian, 1; South American, 1; 
Danish, 1 ; Russian, 1 ; Cuban, 1. The ages ranged from 21 to 
52. Bv ages the following data was obtained: 







































































Total: 18 none; marked 36; medium 27; slight 46. Per- 
centage: 14.1 none; 28.3 marked; 21.2 medium; 36.2 slight. 

In studying these figures it will be noted the largest number 
of cases of interstitial gingivitis occurred between the ages of 
21 and 30, the period of life at the constructive stage when the 
disease should not be present. Those over forty were nearly all 
officers who took better care of the mouth. It must be also noted 
these men lived most of the time in the open air. In the Amer- 
ican army mostly young men are enlisted. It will be seen that 
the effect of climate and food is very severe. 1 

Even in moderate temperatures where changes of climate 

The Dental Summary, 1903. 


have taken place, strong persons, after long exposure to such 
temperatures, undergo a certain degree of lassitude, diminution 
of appetite and impairment of functions of digestion, respira- 
tion, circulation and metabolism. On the other hand, it is also 
true that weak persons may gain in weight and the functions of 
the mind and body be much improved. 

The sudden changes in temperature and atmospheric pres- 
sure, such as mountain climbing, balloon and aeroplane ascen- 
sion, may cause great exhaustion, palpitation of the heart, ir- 
regular breathing, unconsciousness, and sometimes vomiting, 
with bleeding of the gums. It is claimed by some research 
workers that the capillaries of the lungs are unable to take up 
sufficient oxygen from the highly rarified air. According to 
the investigations of Schumburg and Zumtz it appears that a 
given amount of labor calls for a greater amount of oxygen in 
an increased elevation than in a lower level. It would seem, 
however, that the sudden changes from moderate to extreme 
cold or heat act upon the body in such a manner that the elim- 
inating organs are unable to adjust themselves quickly to the 
new environment. The result of this is that autointoxication 
takes place and faulty metabolism is produced. 

During the building of the Grornergrat Railway in Switzer- 
land, it was found that at a height of three thousand meters, 
the capacity of the laborers was diminished to one-third. Ac- 
cording to the researches of Egger, Miescher and others, a so- 
journ in high altitudes leads, after a short time, to an increase 
in the number of red cells and a greater haemoglobin content in 
the blood. 

Hafner 2 of Zurich has recently shown that "the engineers 
and workmen on the Jungfrau railway, obliged to remain a con- 
siderable time at altitudes of about 2,600 meters above the sea 
level, are liable to a disagreeable complaint. After eight or ten 
days they are seized with violent pains in several teeth on one 
side of the jaw, the gums and cheek on the same side becoming 
swollen. The teeth are very sensitive to pressure, so that mas- 
tication is extremely painful. These symptoms increase in 

'Die Natur, 1900. 


severity for three days and then gradually and entirely dis- 
appear. It seems to be purely a phenomenon of acclimatization. 
All new comers pass through the experience and the disorder 
never recurs." The influence of heat, of cold and of the baro- 
metric pressure shown in a lesser degree in "mountain fever" 
produce systemic disturbance of metabolism which, causing 
autointoxication, markedly affect the alveolar process, producing 
interstitial gingivitis. 

The author has examined the mouths of the workmen on the 
Jungfrau, Gornergrat and Pillatus Railways at various times 
and can confirm the statements made in regard to the condition 
of the men as stated above. The quality of food, the unhygienic 
condition of the mouth and high altitude have acted severely 
upon the alveolar process, causing the teeth to loosen and drop 
out. While the pathology is similar to scurvy, the other consti- 
tutional symptoms, associated with scurvy, are not observable 
in these patients. 

When the Government authorities made their report on the 
survey of the State of Minnesota many years ago, they made 
the claim that it was impossible for human beings to live the 
entire year in that state owing to the extreme cold in winter. 
It is now known that in the Northwest, owing to the extreme cold 
in winter, people who live in exceedingly hot rooms suffer from 
the extremes of cold and heat and are subject to more severe 
interstitial gingivitis than those in more moderate temperatures 
in the United States. 

The results of these extremes in temperature produce many 
affections of the heart from a want of quick adjustment of the 
eliminating organs to the new environment. In high altitudes 
and cold climates, the skin contracts and elimination of the body 
waste is thrown upon the internal organs, and vice versa in 
warm climates. 

The result is that in these sudden extremes, the functions of 
the body are slow in adjusting themselves to environment, nutri- 
tion is interfered with, vitality is lowered and the structures of 
the body are affected in the order of their sensibility to auto- 
intoxic states. The peripheral nerves are usually the first in- 
volved; then the arterial coats and the blood stream are inter- 


fered with. Transitory structures and end organs thus receive 
the first impulses of faulty metabolism. 

This sets up an inflammation in the capillaries of the alveolar 
process. No matter how short a time the cause may exist, if the 
inflammation is once set up, owing to its peculiar action on the 
alveolar process (even though the cause be removed), inter- 
stitial gingivitis becomes chronic and the destruction of tissue 



Scurvy is due to poor food and improper hygiene. Insuffi- 
cient alternation of food, impure air, want of bodily exercise, 
ennui and uncleanliness combine to form the causes of this dis- 
ease. Previous to the introduction of canned goods, sailors on 
long voyages, prisoners and others under confinement were 
subject to scurvy. Lunatics, idiots or persons who have had 
long illness, and find it difficult to regulate their diet, are now 
most prone to it. Anaemic convalescents from protracted fevers 
suffer from it. Bottle-fed babies and occasionally those fed at 
the breast on non-nourishing milk are prone to the disease. 

In the British Arctic Expedition of 1875-76 over forty-eight 
per cent of the men suffered from scurvy. When the potato crop 
failed in Ireland, in 1846, scurvy became prevalent. In the 
Crimean war 23,000 cases occurred among the French troops 
alone. Scurvy contributed over fifteen per cent to the death rate 
in the late civil war. It occurs among the Klondyke miners. 

Thomas Barlow found scurvy associated with rachitis. Sun- 
derland found that rachitic diathesis was a very strong factor. 
Jacobi reports forty cases of scurvy and rachitis. Babies in 
good families brought up solely on the proprietary infant foods 
are prone to scurvy. They lose their appetites, become pallid, 
perspire freely, have diarrhoea, the mouth becomes sore, with in- 
flamed mucous membrane and gums. Purpura and hemorrhages 
of mucous membrane are common with pain and swelling of the 

Just how far scurvy may be associated with extreme changes 
in climate in relation to interstitial gingivitis is an open question, 
but soldiers going from one climate to another, as exampled by 
American soldiers to Cuba and the Philippines, and British sol- 
diers to South Africa and India, are more subject to scurvy 

Brit. Epidemiological Society, Feb. 19, 1904. 


from improper food than native soldiers. Mayer Coplans * of 
the British Army Medical Sendee states, in regard to the South 
African War, that scurvy developed among the local population, 
in the concentration camps, fed upon Government rations which 
were of fairly good quality. The concentration of native women 
and children in camps containing about 5,000 persons, forty- 
eight per cent of children under twelve years of age contracted 
the disease. Among adults the women were to the men as three 
to one. Enclosed by barbed wire, the camps, though open and 
airy, were securely isolated. The conditions being identical the 
varying incidence of scurvy was remarkable. Between March, 
1901, and January, 1903, with no cases at Standerton or Volks- 
rust, there were one hundred Europeans and one native attacked. 
Among the soldiers at Standerton and the 22,000 European 
patients admitted to the hospital there was but one ; among the 
natives in the service of the troops there were attacked 32 per 
cent of 400 muleteers, 22 per cent of those attached to the Hus- 
sars and the Royal Artillery, 87 per cent of the scavengers en- 
gaged in removing carcasses of animals, 17 per cent of the 
porters and about 50 per cent of the muleteers in the employ of 
the repatriation department. 

The heaviest incidence of scurvy was after the close of the 
war and when all restriction on food had been removed. In fact, 
it had no relation whatever to the food but was almost every- 
where directly in proportion to the neglect of cleanliness, of 
which the natives had not the most rudimentary notions, espe- 
cially as regards the hygiene of the mouth. Even the outbreak 
among the burghers at Middleburg followed overcrowding and 
neglect of sanitation. 

A. E. Wright, in discussing the subject, said filthy habits 
were not peculiar to the Kaffirs, and were not always accom- 
panied by scurvy, which occurred in the nurseries of the rich and 
in nursing homes. Scurvy was essentially an acid intoxication, 
a reduction in the alkalinity of the blood which can be observed 
long before the grosser manifestations, alike in the adult and 
infantile forms. A large proportion of the troops returning from 
South Africa were scorbutic in the latent stag'e. 


K. B. Goadby also, in a discussion of the subject, said he had 
not seen any scurvy at the Dreadnaught Hospital, but had met 
much pyorrhoea alveolaris, a disease endemic and occasionally 
epidemic in West and Central Africa, the Transkei, the Philip- 
pines and other places. This condition of the gums and the rapid 
recovery of the patients under antiseptic measures resembled 
that found in scurvy. 

Coplans pointed out in reply that it required months for 
its development, for the members of the corps that suffered 
most were recruited in their homes in October and the corps was 
dissolved in December, the disease breaking out soon after their 
arrival in the camp. Recovery followed rapidly on purely local 
treatment in the way of buccal antiseptics without any attempt 
to influence the blood. 

The term "scurvy" frequently employed in this discussion is 
applied to the disease of the mouth, especially in relation to the 
gums. Nothing is said in regard to other symptoms of the body, 
which would be necessary in order to make a clear diagnosis of 
scurvy. The logical inference is that such were not present. 

Polar expeditions led to the conclusion that a diet of fresh 
or even raw meat, without any food or vegetables whatever, 
and associated with hardship, dirt and misery, or one consisting 
entirely of tinned, preserved and sterilized foods of the highest 
quality but with no fresh food, animal or vegetable, did not pro- 
duce symptoms of scurvy, while scurvy appeared when, along 
with potatoes, etc., and daily doses of lime juice, the bulk of the 
food consisted of ordinary salt beef or pork. Until the recent 
Antarctic expedition, from that of Nordenskjold in the Vega, 
none had been attacked by scurvy except that of Jackson, whose 
men remained on board the ship where they had lime juice, po- 
tatoes, etc., but refused the coarse, even "gamey" bear's flesh, 
on which alone the exploring party subsisted. All were attacked 
with scurvy, two, indeed, dying. The Laplanders of Finland 
bartered for farinacea, etc., but ate their fish putrid by prefer- 
ence, and suffered much from scurvy. 

In scurvy there is inflammation and bleeding gums; the 
gums puff up, thicken and bleed easily; the teeth become loose 
and sore upon mastication ; a disagreeable odor comes from the 


mouth; salivation or ptyalism results from irritation of the 
teeth, as well as scorbutic anaemia; the patient is languid or 
tires, perspires freely upon exertion, has shortness of breath and 
palpitation of the heart ; the face is ashy gray, becoming paler 
each day ; hemorrhage takes place in different parts of the body, 
especially beneath the skin, in the muscles and beneath the peri- 
osteum, as well as in the joints. This often gives considerable 
pain and sometimes causes inflammation, with resultant pus in- 
fection. Occasionally hemorrhage takes place in the internal 
structures. The temperature varies and both febrile apyretic 
states occur. 

On the other hand, the symptoms observed in interstitial gin- 
givitis are confined to the gums and alveolar process. There 
are no constitutional symptoms. This disease was formerly 
known as pyorrhoea alveolaris because the disease was not recog- 
nized until pus was observed about the teeth. It frequently ex- 
ists for years before pus is noticed. All the teeth may be lost 
without pus. 

From what has been said, it would seem rather difficult to 
assume that these mouth conditions herein described were en- 
tirely due to scurvy. Changes in climate and environment must 
be considered in relation to the interstitial gingivitis as well as 
unhygienic conditions. 

It is common to find scurvy in private and state institu- 
tions where many people are confined, due to a monotony of food. 
The following scorbutic case was referred to me by Dr. George 
W. Johnson : A twenty-five-year-old American was admitted to 
Cook County Hospital for the Insane December 2, 1892, suffer- 
ing with melancholia, attended by delusions of persecution and 
suicidal tendencies marked by refusal of food. June 1, 1896, he 
again began to refuse food, but took liquid diet on persuasion. 
June 29, the patient was transferred to the hospital because of 
his emaciation and scorbutic symptoms were discovered. July 
18, the constitutional and local symptoms of scurvy were well 
marked. The teeth were covered with sordes and loosened. 
Under antiscorbutic treatment these symptoms had fully dis- 
appeared by August 13. Through the kindness of Dr. Johnson 
I was allowed to see this patient. I found none of the teeth very 


loose, showing- the disease was superficial. I removed two teeth 
that were decayed and the most loose. These were prepared 
for the microscope in the usual way. The gums and peridental 
membrane were in an active state of inflammation. Small blood 
vessels were observed in different localities with round cell 
infiltration extending into the tissue. The root of the right 
superior second bicuspid, with peridental membrane attached, 
showed active inflammation about an artery which had thick- 
ened, and an area of tissue degeneration, forming an abscess. 
The interstitial gingivitis due to scurvy, drug or self-poisoning 
has the same pathology. 



The retrograde disturbances of nutrition lead to degeneration 
of the affected tissue. Tissue infiltrations are due to deposits in 
the tissues of pathologic substances which have either been 
formed within the body or introduced into it from without. 
These disturbances of nutrition may affect the alveolar process 
during its period of development and growth, but more partic- 
ularly in a fully developed state. 

Poisons may be divided according to their action into three 
groups : First, those producing local tissue changes ; second, 
those acting injuriously upon the blood; third, those affecting 
chiefly the nervous system and the heart without producing 
recognizable anatomic lesions. The poisons of all these groups, 
acting on the alveolar process, either by producing irritation of 
the blood vessels or by disturbing nutrition because they are 
stored in the tissue by producing trophic and vasomotor changes 
through their action on the nerves, work toward the ultimate end 
of its destruction. 

All causes which bring about stasis of blood in the capillaries, 
such as inflammation, pressure, hemorrhage or blocking the 
venous outflow from the part, will cause arrest of nutrition. 
Again, if the arterial supply be cut off from any cause, destruc- 
tion of the process will take place. Arrest of circulation need 
not be permanent. It suffices for its evil effect if it persists for a 
certain time. The more highly specialized a tissue, the briefer 
its vitality when deprived of blood ; thus, when the blood supply 
is cut off, absorption of the alveolar process takes place before 
the circulation can be re-established. This is more than likely 
to take place in the alveolar process since it is a doubly transi- 
tory structure and an end organ. 

Under the influence of poisons of all kinds, the alveolar proc- 
ess is liable to be absorbed. The result depends on the condi- 
tion of the patient and the severity of the poison. The lowering 


of vital resistance is proportional to the depth of the poisoning, 
and the weakened condition of the tissue invites microbic infec- 
tion and multiplication, affording a suitable soil for invading 
micro-organisms which lead to the development of pyorrhoea 
alveolaris. This is true of the poisons entering the arteries of 
the process which cause an increased pressure of blood. 

The toxins which leave an indelible stamp upon the alveolar 
process are divisible into those belonging to the condiments, 
foods, beverages, drugs, and those arising from occupation. 
Tobacco, alcohol, tea, coffee, opium, cocoa, cocaine, as well as 
mercury, lead, brass, potassium iodid, phosphorus, sodium 
chloride and other metals. 

With tobacco, as with alcohol and opium, the statistic method 
generally proves fallacious when applied to degenerative effects. 
The most careful researches show that the typical effects occur 
as a rule after long continued use of tobacco, sometimes not 
until twenty years or more. While many smokers reach old age, 
many fail to live to old age because they are smokers. The skin 
is subject to itching and reddening; the nerves of taste are 
blunted and patches develop in the throat; loss of appetite, 
epigastric fulness, pain, vomiting and disturbance of bowel func- 
tion are common. Menstrual disturbance occurs in women, and 
in female cigar-makers abortion and pluriparity are frequent. 
The sexual appetite is impaired, and sometimes sterility and 
impotence occur. Disturbed heart action, palpitation, rapid and 
intermittent pulse, precordial anxiety, weakness, faintness and 
collapse, with sclerosis of the coronary arteries of the heart and 
left ventricular hypertrophy occur often. Cigars and cigarettes 
produce irritation of the nose and mucous membrane, diminished 
smell, chronic hyperemia of the epiglottis and larynx, and some- 
times of the trachea and bronchi, predisposing to tuberculous 
infection. Nicotine amblyopia is common, with central disturb- 
ances of the field of vision and slight color blindness. Often 
there is disorder of the ear tubes and congestion of the drum, 
with loss of auditory power and consequent noises in the ear. 
The central nervous system is affected. In high schools non- 
smokers progress faster than smokers. Child smokers, from 
nine to fifteen years of age, exhibit less intelligence and more 


laziness or other degenerative tendencies. Adults have head 
pressure, sleepiness or drowsy stupor, depression, apathy and 
dizziness. There may also he ataxic symptoms, paretic weak- 
ness of bowels and bladder, trembling and spasms. Tobacco 
insanities, though comparatively rare in smokers, are common 
in snuffers and still more in chewers. 1 In the precursory stage, 
which lasts about three months, there are general uneasiness, 
restlessness, anxiety, sleeplessness, and mental depression, often 
of a religious type. After this occurs precordial anxiety, and 
finally the psychosis proper, consisting of three stages : 1. Hal- 
lucinations of all the senses, suicidal tendencies, depression, at- 
tacks of fright, with tendency to violence and insomnia. 2. Ex- 
hilaration, slight emotional exaltation, with agreeable hallucina- 
tions after from two to four weeks' relaxation, again followed 
by excitement. 3. The intervals between exaltation and depres- 
sion diminish, and the patient becomes irritable, but otherwise 
not alive to his surroundings. Perception and attention are les- 
sened. The patient may be cured in five or six months if he stops 
tobacco during the first stage. In a year or so he may recover 
during the second stage. After the third stage he is frequently 
incurable. As the patient becomes (especially by the use of the 
cigarette) an habitue before puberty, the proper development 
and balance of the sexual and intellectual system is checked. 
These patients break down mentally and physically between 
fourteen and twenty-five. The moral delinquencies, other than 
sexual, are often an especial tendency to forgery and deceit of 
parents. Frequently the insanity of puberty (hebephrenia) is 
precipitated by tobacco. The cigarette, if used moderately, may 
be a sedative, but, as used, is a stimulant, and is often made of 
spoiled tobacco, resembling in reaction morphine, and acting on 
animals in a somewhat similar manner. As tobacco turns the 
salivary glands into excretory glands, it leads to imperfect di- 
gestion of starch and to consequent irregular fermentation in 
the bowels, thus at once furnishing a culture medium for mi- 
crobes, from which to form violent toxins, and likewise creating 
leucomaines, to damage a nervous system overstimulated by 

Annual of the Universal Medical Sciences, 1895. 


nicotine. This is one great reason why those who use snuff and 
chew tobacco become insane more frequently than smokers, 
albeit these last are not exempt. 

Statistics from the female employes of the Spanish, French, 
Cuban and American tobacco factories, while defective and 
somewhat vitiated by the coexistence of other conditions pro- 
ducing degeneracy, support the opinion that the maternal to- 
bacco habit (whether intentional or the result of an atmosphere 
consequent on occupation) is the cause of frequent miscarriage, 
of high infantile mortality, of defective children, and of infantile 
convulsions. Tobacco, therefore, in its influence on the paternal 
and maternal organism, exhausts the nervous system so as to 
produce an acquired transmissible neurosis. 

Alcohol has been repeatedly charged with being the greatest 
factor in degeneracy. The influence of alcohol on the individual 
must first be studied to determine its potency and method of 
action as a cause of race deterioration. Careful medical re- 
searches have shown that alcohol produces a nervous state 
closely resembling that induced by the contagions and infections, 
and often accompanied by mental disturbance. The acute nerv- 
ous state to which the term "alcoholism" was applied by Mag- 
nus Huss has all the essential characteristics of the nervous 
state due to the contagions and infections or mental exhaustion. 
The action of alcohol may be limited to the central nervous sys- 
tem and thus produce hereditary loss of power. It may cause 
changes or degeneracies in the peripheral nerves which in the 
offspring find expression in spinal cord and brain disorder 
through extension of the morbid process. But for its deterio- 
rating effects on the ovaries and testicles alcohol would be a 
most serious social danger. Through these, however, it tends 
to prevent the survival of the unfit rather than to develop 

Professional tea-tasters have long been known to suffer from 
nervous symptoms. Very early in the practice of their occupa- 
tion the head-pressure symptoms of neurasthenia appear. 
Tremor also occurs early. While changes in the optic nerve 
have not been demonstrated beyond a doubt, still eye disorders 
have been observed in the pauper tea-drinkers of the United 


States and the tea-tasters of Russia, indicating similar changes 
to those produced by tobacco and alcohol. The tea-cigarette 
habit has these effects. Bullard 2 finds that tea has a cumulative 
effect. In his experience, toxic effects are not produced by less 
than five cups daily. The symptoms manifested are those of 
nervous excitement resembling hysteria, at times almost amount- 
ing to fury ; nervous dyspepsia ; rapid irregular heart action ; 
heart neuralgia ; helmet-like sensation and tenderness along the 
spine. James Wood 3 of Brooklyn found that ten per cent of 
those under treatment at the city hospitals exhibited similar 
symptoms. Of these sixty-nine per cent were females, and every 
symptom ascribed by Bullard to tea was seen by Wood in his 
cases, who also found that the women manifested irregularities 
in menstruation of a neurasthenic or hysterical type. He found 
that these symptoms were produced by one-half of the quantity 
of tea charged with these effects by Bullard. The Lancet, sev- 
eral years ago, from an editorial analysis of the effects of tea- 
tippling, took the position that in no small degree nervous symp- 
toms occurring in children during infancy were due to the prac- 
tice of the mothers, both of the working and society class, in- 
dulging in the excessive use of tea, the excess being judged by its 
effects on the individual and not by the amount taken. Convul- 
sions and resultant infantile paralysis were frequently noticed 
among the children of these tea-tipplers. Observations among 
the factory population and the workers in the clothing sweat- 
shops show that tea neurasthenia, presenting all the ordinary 
symptoms of nervous exhaustion, is especially common. It is 
evident that tea produces a grave form of neurasthenia readily 
transmissible to descendants. In addition to its effects directly 
upon the nervous system, tea tends to check both stomach and 
bowel digestion, and this increases the self -poisoning which is so 
prominent a cause, consequence and aggravation of these nerv- 
ous conditions. 

Coffee exerts an action very similar to that of tea, although 
the nervous symptoms produced by it are usually secondary to 
the disturbances of the stomach and bowel digestion. Coffee 

Annual of the Universal Medical Sciences. 1889. 


produces tremor, especially of the hands, insomnia, nervous dys- 
pepsia and helmet sensations. With the exception of certain dis- 
tricts of the United States coffee abuse is not carried to such an 
extent as tea, albeit in these, as in some portions of Germany, the 
habit is an excessive one. The conditions described result in 
Germany as frequently as they do in the United States. Mendel 4 
finds that in Germany coffee inebriety is increasing and sup- 
planting' alcohol. Profound depression, with sleeplessness and 
frequent cortex headache, are early symptoms. Strong coffee 
will remove these temporarily, but it soon loses its effect and 
they recur. The heart 's action is rapid and irregular, and nerv- 
ous dyspepsia is frequent. L. Bremer of St. Louis has observed 
similar conditions among both Germans and Americans there. 
Opium seems to be the Charybdis on which the human bark 
strikes when escaped from the Scylla of alcohol. Its abuse as a 
narcotic is much older than is generally suspected even among 
the English-speaking races. Murrell over ten years ago demon- 
strated that the inhabitants of the Lincolnshire fens had long 
employed opium as a prophylactic against malaria. The ratio 
of insanity in these regions proved to be very great. The same 
conditions obtained in central malarial regions of New Jersey 
and Pennsylvania, where the use of strong infusions of the 
poppy was common. The statistics of Rush 5 as to opium-caused 
insanity in Pennsylvania indicate that the percentage of Amer- 
ican opium abuses at the beginning of the nineteenth century 
was very great. The drug differs in two important aspects from 
alcohol — it is nearer in chemical composition to nerve tissue, 
and the tendency to its use may be transmitted by the mother 
directly to the fetus, since it passes through the placenta very 
often unaltered. Opium is a more dangerous factor of degen- 
eracy than alcohol, since the opium habitue must be in a contin- 
uous state of intoxication to carry on his usual avocation, while 
abstinence from alcohol is perfectly compatible with proper 
work on the part of the alcoholist. The opium habit is increased 
by the propaganda carried on by the habitues, who justify their 
position by urging the use of opium for any ailment, however 

* Neurologisches Centralblatt, 1887. 
6 Observations on the Brain and Mind. 


trifling. Opium, like alcohol, causes nervous exhaustion similar 
to but greater than that of the contagions and infections. From 
the affinity of opium to nerve tissue ; from its tendency to stim- 
ulate the heart, thus causing increased blood supply to the brain ; 
from its action on the bowels and the increased resultant work 
of the liver, this nervous state is much intensified. Opium does 
not interfere with the structure and fecundation of the ovary 
and testicles like alcohol, hence the danger of the opium habitue 's 
children surviving. Opium, when smoked, stimulates the re- 
productive apparatus and thus greatly increases the number of 
degenerates due to this habit, although the defects due to the 
inheritance of the habit and their consequences lessen survival. 

While coca took its place but recently among the toxic causes 
of degeneracy, it was a factor of Peruvian degeneration long 
ere the discovery of America. Forty-three years ago 6 Euro- 
peans or people of European origin in different parts of 
Peru had fallen into the coca abuse. A confirmed chewer 
of coca, called a coquero, becomes more thoroughly a slave to 
the leaf than the inveterate drunkard is to alcohol. Some- 
times the coquero is overtaken by an irresistible craving 
and betakes himself for days together to the woods and 
there indulges unrestrainedly in coca. Young men of the 
best families of Peru are considered incurable when addicted 
to this extreme degree, and they abandon white society 
and live in the woods or in Indian villages. In Peru the term 
"white coquero" is used in the same sense as irreclaimable 
drunkard. The inveterate coquero has an unsteady gait, yellow 
skin, quivering lips, hesitant speech and general apathy. The 
drug has assumed an unusual prominence in the field of degen- 
eracy since the discovery of its alkaloid, cocain. 

In both Europe and the English-speaking countries the world 
over a habit has resulted which, while much overestimated, is 
undoubtedly growing and aggravating as well as producing de- 
generacy. Many of the cases reported as due to cocain are, how- 
ever, chargeable to the craving of the hysteric or neurasthenic to 
secure a new sensation, or the desire on the part of the opium or 

6 Johnson, Chemistry of Common Life, Vol. II. 


whisky fiend to try a dodge of forgiveness by friends. The habit 
is very frequently induced by patent medicines taken to cure 
catarrh by the neurasthenic or to cure nervousness by the hys- 
teric as well. As deformities of the nose passages predispose to 
"catarrh," patent medicines for local application containing 
cocain are frequently employed in the treatment of this supposed 
constitutional disease, with the result of aggravating the original 
degeneracy. The youth under stress of puberty frequently 
ascribes all his ills to catarrh, and for it often employs snuffs 
containing cocain, and his nervous condition is much aggravated 
thereby. Among the nostrums urged in the newspapers and 
magazines for this condition so often resultant from nerve stress 
alone is a snuff containing three per cent of cocain. From the 
description given by Johnson of the coquero there can be no 
doubt that tramps, wandering lunatics and paupers result from 
this habit to give birth to degenerates in the next generation. 

It is a widespread opinion among dentists that in toxic cases 
the gums are the first tissues involved. The fact is, however, 
that when the salts of mercury are taken into the system, as 
noted elsewhere, they act directly upon the central nervous sys- 
tem; later occur nausea and vomiting, tremor in the arms and 
hands. Besides local nerve inflammation (neuritis), mercurial 
and brass poisoning produce paralysis agitans, and lead poison- 
ing, drop wrist, etc. 

Excessive secretions of the glands of the body, especially the 
salivary glands, later occur with rise in temperature, gingivitis 
with periosteal and peridental membrane swelling, thickening 
of the gums and loss of teeth. The central nerve system disturb- 
ance affects all other structures. Inflammation of the mucous 
membrane of the mouth, as well as of the gums, and of the ali- 
mentary canal, frequently occurs with sloughing of tissue. The 
kidneys become involved, and are unable to carry off the effete 

The cachexia, which resembles that of scurvy, is characterized 
by great debility, anemia, emaciation, alopecia, atrophy and 
coarseness of the nails, with pain in the muscles and joints. 

Mercury is eliminated by all excretory organs for which it has 
a great affinity. The soluble salts pass out by the bowels. So 


long as the excretory organs of the body eliminate mercury, the 
tissues are not affected. Small doses are eliminated, but con- 
tinuation of dosage soon involves the nervous system, and after- 
wards the tissues of the body, especially the jaws. The first 
effect of mercury upon dogs is to produce vivacity and anima- 
tion. This lasts for two or three days, when the limbs begin to 
tremble. The kidneys and bowels act at first freely. At the end 
of seven or eight days paralysis agitans occurs. There is con- 
stant trembling, whether awake or asleep ; loss of appetite, with 
slight rise of temperature. At the end of two weeks the gums 
become inflamed at the margins. If the drug be continued, death 
occurs in about three weeks. The loss of flesh is remarkable. 
Miners working in mercury mines, and looking-glass makers, are 
all affected to a greater or less extent. The nervous system is 
always involved. The kidneys become diseased. The hair drops 
out. The miners think it a happy issue from their trouble when 
they have lost all their teeth, or even the molars. They are 
henceforth exempt from suffering so far as the teeth are con- 
cerned. Many are toothless at thirty-five. 

Mercury taken by the mouth is found in the urine in two 
hours, and in the saliva in four hours. It appears in the urine 
fourteen hours after it has been applied to the skin. 7 Although 
it is believed to have passed entirely out of the system, it has 
been found in the brain, liver, kidneys and muscles. It is claimed 
that, like lead, it forms combinations with albuminoids in the 
tissues, for a time remaining inert, to be subsequently oxidized 
and returned to the circulation as an active poison. While a 
single dose of mercury may be rapidly eliminated from the sys- 
tem, repeated small doses distributed over a long period are not 
so eliminated on account of the thickness and occlusion of the 
walls of the capillaries, producing endarteritis obliterans, hence 
more or less of it is deposited in the tissue. 

Lead enters the system through the alimentary canal, skin 
and respiratory tract. A longer time is required to produce 
plumbism (lead poisoning) than mercurial poisoning. Lead is 
stored up in the system in minutest quantities for an indefinite 

'Twentieth Century Practice of Medicine, Vol. Ill, page 935. 


length of time. Its effects are not manifest until the central and 
peripheral nervous systems have become involved, as evinced 
by the effect of plumbism upon the wrists. Occasionally, the 
chief seat of deposit is the liver or muscles. It is chiefly elim- 
inated through the kidneys, and very slightly through the liver 
and salivary glands. Not until a considerable length of time has 
elapsed is lead traceable upon the gums. This usually occurs 
about the lower incisors and cuspids. This deposit (lead sul- 
phid) is always in the tissue outside of the blood vessels. Plumb- 
ism causes trembling, nausea and vomiting. The patient loses 
flesh, becomes anaemic, and has great resultant debility. 

The lead circulating in the capillaries accumulates, owing to 
impeded circulation resultant on the thickening of the coats of 
the vessel, producing occlusion. A bluish line upon the gums 
indicates that the system is completely saturated. Like mercury, 
lead collects in the mucous membrane upon the inside of the 
mouth, producing blue patches from a line to one-half an inch 
in length. Lead not only produces local irritation, but affects the 
peripheral nerves as well, producing atrophic changes ; upon the 
capillaries a thickening of the inner coat results in endarteritis 

Lead produces in those exposed to the fumes a systemic nerv- 
ous exhaustion, characterized by local paralysis about the wrist, 
as well as the general symptoms of profound systemic nerve 
tire. This may result, as was pointed out nearly half a century 
ago, 8 in acute insanity of the confusional type followed very often 
by mental disorder of a chronic type resembling paretic de- 
mentia. In some cases the patient recovers from the acute 
insanity to suffer thereafter from epilepsy. In other cases ° an 
irritable suspicional condition also results, in which the patient 
may live for years, marry and leave offspring. This last condi- 
tion and the epileptic are the most dangerous as to the produc- 
tion of degeneracy. The women employed in the pottery fac- 
tories in Germany suffer, according to Rennert, 10 from a form 
of lead-poisoning which produces decidedly degenerative effects 

8 Tanquerel des Planches, Lead Diseases, American Edition, 1848. 
" Kiernan, Journal of Nervous and Mental Diseases, 1881. 
10 American Journal of Obstetrics, Oct., 1882. 


upon the offspring. These women have frequent abortions, often 
produce deaf-mutes and very frequently macrocephalic children. 

Brass-workers suffer from a nervous condition very similar 
to that produced by lead. Hogden u of Birmingham and Moyer 12 
have called attention to the grave forms of nervous exhaustion 
produced among brass-workers. The period during which the 
patient is able to pursue the occupation without breaking down 
is longer than that of the lead-workers. Women, like men, are 
exposed to this condition. The chief effects produced, so far as 
the offspring have been observed, are frequent abortions and 
infantile paralysis. The green gum is an early symptom. 

Potassium iodide exerts a like toxic influence to lead and 
mercury, as its pathology is similar thereto, but it is of infre- 
quent occurrence. 

The employment of women in match factories and tenement- 
house sweat-shops is growing. The chief toxic effect of phos- 
phorus is not the localized jaw necrosis. This is but an evidence 
of the progressive system saturation with phosphorus, and bears 
the same relation to the more dangerous effects of phosphorus 
that the "blue gum" does to the systemic effect of lead. 

In adults, excess of sodium chloride in the blood from con- 
sumption of salt meats and fish has been noted with scurvy. 
For this reason Bawls, of Cincinnati, Ohio, believed that an 
excess of salt in the system produced gingivitis. Languor, de- 
pression, anaemia, with a rise of temperature, and enlarged 
joints with soreness are the first symptoms. 

The effects of this disease upon the system are almost identical 
with those of mercury and lead. Bruise-like (purpuric) erup- 
tions occur upon the skin and mucous membrane, on the serous 
membrane (notably the pleura, pericardium, meninges and 
synovial linings of the joints), mucous membrane of the mouth, 
stomach, intestines and bronchi. 

Owing to the anaemia, vascular weakness and altered compo- 
sition of the blood, edema is common both in the lungs and in the 
submucous and subcutaneous tissue, especially the feet and legs. 
The gums begin to swell with redness and fibrous thickening of 

11 Birmingham Medical Review, Jan., 1887. 

12 Medicine, May, 1904. 


the deep layer, which cause protrusion, especially in the cases of 
degenerates. The blood vessels, especially the capillaries, be- 
come thickened, in some cases they are occluded, or erosion and 
ulceration occur. The patient becomes decidedly pale and 
markedly debilitated. The skin is dry and blanched. General 
emaciation is evident. 

The mucous membrane and gums become swollen and bleed, 
stomatitis ulcerans results in greater or lesser degree. The 
tongue is at first swollen, then it becomes dry and hard. The 
gums are at first red and swollen. They bleed easily upon the 
slightest touch. Later they become pale and are irregularly 
larger, somewhat fungoid and friable, protruding between the 
teeth. They are quite tender to the touch. Ulcers appear on 
the buccal surfaces. The stomach becomes irritable, nausea and 
vomiting are common. Constipation occurs early and diarrhoea 
later appears. 



Every day we hear or read of individuals, in the prime of 
life and to all intents in good health, dying suddenly. Post- 
mortem reveals nothing whereby we may satisfy our minds as to 
the actual cause of death and the case passes into medical his- 
tory as an obscure condition. If we were familiar with auto- 
toxic states, I am sure many of these seemingly obscure condi- 
tions could be accounted for. Autointoxication is the rock upon 
which the human bark is wrecked and of which physicians know 
so little. 

The human organism even in its normal state is prone to its 
own destruction by poisons. These poisons are formed within 
the organism itself or are taken into it in foods, liquids and 

Selmi, the Italian toxicologist, gave the name of ptomaines 
to basic substances formed in putrefying animal matter. From 
their similarity to vegetable alkaloids, the ptomaines are often 
spoken of as putrefactive or animal alkaloids. Leucomaines are 
animal alkaloids formed by the metabolic processes of the 

The processes of intestinal putrefaction and the formation of 
physiologic and pathologic alkaloids afford an explanation of the 
pathogenesis of many diseases, the origin of which was obscure 
until recent investigations gave us the key by which their true 
nature may be understood. 

We must admit the great impetus given to disintegrating 
processes in organic matter by bacteria. In no part of the body 
is this more true than in the alimentary canal. During the proc- 
ess of digestion, changes of a chemic, putrefactive and ferment- 
ing nature take place in the small intestine, which give the op- 
portunity for the formation of poisonous substances, and these, 
when absorbed have an injurious effect on the system. There 
is some protection against this, however, if the liver, kidneys, 


lungs and skin (the great sewers of the body) be not too deeply 
involved. When these poisons are not eliminated, or when any 
one of the eliminating organs becomes diseased and other organs 
are obliged to perform that function, these poisons are carried 
in the blood stream to the remote parts of the body. The organs 
most frequently involved as recognized by physicians, are the 
liver, kidney, heart, brain and eye, but the bony alveolar proc- 
ess, a doubly transitory structure and end organ and the dental 
pulp, which is the most perfect end organ in the body, are the 
first to record symptoms of disease. 

If the disease involves the entire system and all the elim- 
inating organs, the skin, kidneys, bowels and lungs are perform- 
ing, or can be made to perform, their natural functions, many 
of the poisons are soon removed. On the other hand, if any one 
of these organs be involved, the process of elimination is slower, 
as the eliminating organs, which are not involved, must do all 
the work. At best this is imperfectly performed. A great part 
of these poisons is eliminated by the stools. Owing to the slow 
movements of the intestinal contents, much of the poison is ab- 
sorbed by the mucous membrane. In faulty metabolism or tissue 
changes, toxins are produced which are absorbed and pass into 
the lymph and blood vessels. All poisons, producing intoxica- 
tion, whether due to disease, tissue change, fermentation or in- 
fection, are of interest in their relation to interstitial gingivitis. 
Many of these auto-infections are of short duration and their 
intensity is not lasting. On the other hand, the toxic action of 
mercury, lead, brass, and of the products of syphilis, tubercu- 
losis, scurvy, etc., is familiar to all. These poisons are of vital 
importance to the patient and physician, since they act quickly, 
but, from the viewpoint of the stomatologist, autointoxications 
of slow progress are the ones of vital importance. These sub- 
stances are taken directly into the blood vessels and carried 
throughout the system. This has been repeatedly proven by 
Bouchard. 1 

That man is born free from microbes, was first demonstrated 
bv Metchnikoff. Soon after birth the skin and mucous membrane 

Autointoxication in Disease. 


become infected, either from the air or water used in bathing or 
both. On an examination of the intestinal contents an hour after 
birth, during warm weather, bacteria were found. Usually bac- 
teria are not described until from twelve to twenty hours after 
birth. Micrococci and bacilli flourish independently of food, for 
they are found in the alimentary canal before nourishment has 
been taken. These microbes change in character when mother's 
milk or other foods are given the child. The bacillus bifidus 
appears with mother's milk. The colon bacillus, streptococci, 
staphylococci, lactic acid bacillus, etc, with cow's milk. Later, 
with the changes in diet, whether purely vegetable or animal, 
microbic flora grow rapidly in the intestinal tract. Vignas and 
Suckdorf have shown that an adult man passes from 30,000,- 
000,000 to 50,000,000,000 of bacteria daily in the faeces. Many, 
perhaps most of these bacteria, are harmless in healthy indi- 
viduals and the majority are dead. They become exceedingly 
virulent after accidents or injuries, such as gun shot, knife or 
other wounds, strangulated hernia and catarrhal conditions of 
the mucous membrane. Man therefore, is in constant danger of 
being infected. The injury resulting from these micro-organ- 
isms, is not from the bacteria themselves but from their toxins, 
the products which are absorbed. 

Autointoxication, without other pathologic states, is due to 
the absorption from the gastro-intestinal tract, of toxic material. 
Absorption is favored by constipation and the toxic action is 
enhanced by hepatic insufficiency. 

Before considering further the putrefactive changes within 
the intestinal canal, I wish to speak here of a subject about which 
I find little of note by previous writers, namely, changes in the 
digestive tract, due to evolution. Evolution is based upon the 
law of economy of growth, laid down by Aristotle, or use and 
disuse of structures. It is applicable here as in other parts of 
the body. Man, as a whole, has undergone rapid changes and 
is still undergoing greater and greater specialization. In no 
structure of the human body are these changes so great, owing 
to disuse as in the digestive tract. When organs are exercised, 
like the arms of the blacksmith, the hands of the oarsman, the 
legs of the mail carrier, they become enlarged and strong. On 


the other hand, when organs are not used, like the little muscles 
of the ear, the small ribs, the little toes, the blood does not flow 
to the parts in proportion and arrest of development results. I 
have repeatedly shown many times the arrest of the face, jaws 
and teeth in the evolution of man, due to disuse. Civilization, 
by its custom of preparing food and etiquette in eating, has 
caused rapid degeneration of the jaws and teeth, resulting in ir- 
regularities and decay. The mastication of food is a lost art with 
many people, the salivary glands are not excited, arrest takes 
place and saliva containing ptyaline is scanty. Foods cooked 
and swallowed without mastication are taken into the stomach 
with the preparation of first digestion. The gastro-intestinal 
juices are required to perform all the work. Changes in the 
liver, either as to size, quantity of bile secreted or disease cause 
hepatic insufficiency. The same is also true of the pancreas and 
gastro-intestinal juices. The size of the stomach, the length and 
deformity of the intestine and last, but not least, the condition 
of the nervous system and the power of the muscular coats of 
the intestines to expel the contents from the body are to be 

The evolution of the rectum and anus from the placental and 
oviparous mammals is interesting, but is too broad a subject to 
be considered at this time. This evolution, however, in its rela- 
tion to malformations and muscular tonicity, owing to man's 
upright position in his phylogeny must not be lost sight of in the 
study of gastro-intestinal irregularity. 

The sedentary life, due to modes of living, has brought about 
many of these changes. The digestive apparatus has not had 
time to readjust itself to the new environment. Micro-organisms 
and pus germs which have accumulated in the mouth are taken 
into the stomach and intestines with every swallow. These may 
produce injurious results. While the process of digestion con- 
verts the protein or albuminoid substances of the food into pep- 
tones and then into animo acids, the putrefactive bacteria fur- 
ther forms alkaloidal and other poisons which pass into the 

Direct demonstration of this fact has been shown by many 
investigators. Planer, after ligating the colon found H 2 S in the 


blood of the portal vein. Carter has found indican in animals, 
the subjects of intestinal derangements. Bouchard, as well as 
Planer, has observed alkaloids, not only in the tissues, but in 
the blood. Poisons formed, not only in the intestines, but also 
those existing in the tissues, are also observed in the urine. 

That an increase in intestinal putrefaction will cause a large 
quantity of toxic material to pass through the blood into the 
urine has been demonstrated many times. Stadeler in 1848 
found phenol in the urine. Bauman in 1877 found phenol in 
fecal matter. In 1826, Tiedeman and Gmelin discovered a red 
colored substance in the duodenum which proved to be indol. 
Braconnot later found in the urine, indican derived from indol. 
Prof. Metchnikoff of the Pasteur Institute thinks old age is 
chiefly caused by two poisons, phenol and indol which are gen- 
erated in the intestines including such diseases as arterio- 
sclerosis, cirrhosis of the liver, and interstitial nephritis. He 
might also have mentioned heart lesions and interstitial gingi- 
vitis. In 1872, Jaffe injected indol under the skin and afterward 
found indican in the urine. Later experiments by Senator 
failed to find indol in the meconium or indican in the urine of 
newly born infants. It is an established fact today that the 
variation of indican in the urine is governed by the quantity of 
indol in the faeces. In other words, the amount of indican in the 
urine depends upon the activity of intestinal putrefaction. In 
cholera, typhoid fever, intestinal obstruction, Hassal, Gubler, 
Robin, Carter, Jaffe found large quantities of indican in the 
urine. Senator showed indican in the urine in constipation. 

Nencki gave a dog two grains of indol by the mouth, and in 
twenty-four hours there appeared diarrhea. Twelve milligrams 
of a one per cent solution administered subcutaneously to frogs 
caused death. One and five-tenths to two grains of indol ad- 
ministered subcutaneously to a rabbit in twenty-four hours 
proved fatal. By similar experiments Salkowsky found phenol 
and cresol in the urine. Especially was this the case in diarrhea 
and in intestinal obstruction. There is no doubt that in future 
investigations other poisons will be found in the stools and urine 
that produce marked poisonous effect upon the system. Prod- 
ucts of putrefaction formed in the intestines, found in the urine, 


must of necessity circulate in the blood throughout the system. 
There is a natural fermentation going on all the time in the 
intestines. In young and middle aged people, when the excre- 
tory organs are performing their office in a healthy manner, the 
kidneys, bowels, skin and lungs remove the poisonous products 
from the body. "When, however, putrefactive products are 
formed in excess, or the excretory organs have lost their tonicity, 
has the system other means of preventing the accumulation of 
poisons in the blood? Certainly, the liver is intended to per- 
form that office. This has been proven by Schiff. The experi- 
ments by G-. H. Boger with alcoholic extract of rotten meat 
show that when injected into the portal vein it is one half as 
toxic as when introduced into the circulation. 

Bouchard has shown that blood drawn from the portal vein of 
a dog kills a rabbit in a dose from thirteen to sixteen cubic centi- 
meters per kilogram ; that blood removed from the liver requires 
twenty-three centimeters. He has also shown that the injection 
of the extract of 2.5 grams of decomposing meat is sufficient to 
kill a man. 

Many other experiments have been made by scientists show- 
ing similar results. In a summary of the research work, it is 
safe to say that the liver is intended to give protection to the 
system by destroying poisons especially those derived from the 
intestines so that the general system does not receive an amount 
of these poisons above what the excretory organs are able to 

When all conditions work in harmony, that is, when animal 
and man, after years of normal environment, have adjusted 
themselves, disease is less likely to result. When a change of 
environment, such as food, climate and soil, takes place, the 
animal or man becomes more susceptible to disease. Thus 
fifty-five monkeys died of tuberculosis in the Lincoln Park Zoo, 
Chicago, in one year, due to change in food and temperature 
and to confinement. House dogs are more susceptible to dis- 
ease than street dogs. The Indian of North America has been, 
and is, dying rapidly from change in environment and food. 
This is true of other primitive races throughout the world. 


Scandinavians in American cities are very susceptible to disease. 
The same is true of the Negro. 

Many people are still in the primitive stages as regards 
their digestive apparatus. They have inherited an atavistic 
tendency in their large, well-formed jaws, muscles and teeth. 
They masticate food and enjoy it like the carnivora, tearing 
and chewing meat from a hone. The digestive apparatus is 
perfect, the bowels, kidneys, skin and lungs do their work nor- 
mally, and they arc in perfect health. 

Many in whom the digestive apparatus is weak have pro- 
gressed along the line of evolution. These people live a seden- 
tary life one or two generations in advance of the tiller of the 
soil. They are in the transitory stage, not yet adjusted to the 
new environment. A third class, born of neurotic parents, have 
inherited deformed internal organs the secretions and action of 
which are not in harmony with each other. They do not chew 
their food and digestion is impaired. Their nervous systems 
may be impaired from the first, or may become involved as a 
result of faulty digestion and assimilation. 

Studying the three classes singly, it is found that the mem- 
bers of the first class are healthy, that they can eat and drink 
everything and at all times, day and night. They can eat eight 
or ten meals a day, like the King of Portugal, and enjoy them. 
They can drink large quanities of alcohol or beer each day with- 
out difficulty. They are rarely ill. When the senile stage be- 
gins, while there are no marked symptoms, the excretory organs 
fail to perform their work properly. Interstitial gingivitis sets 
in, the teeth loosen, arteriosclerosis, kidney breakdown, uremic 
poisoning result and at from fifty-five to sixty-five death takes 
place from Bright 's disease, diabetes, heart failure or apoplexy, 
the result of excesses. 

The second class easily produce acute gastro-intestinal fer- 
mentation, autointoxication, and are subject to sick headaches, 
acid stomachs, gases in both stomach and bowels and constipa- 
tion. They suffer with headache, migraine and vertigo, and 
often with nervous symptoms. In these cases special foods will 
upset the entire system. Fruits, raw as well as cooked, set up 
fermentation in the small intestines and putrefaction results. 


Coffee, chocolate, cocoa, beer, and the inhalation of tobacco 
smoke will disturb the digestion, produce cold extremities, sick 
headaches in a few hours and not infrequently skin eruption. 

The third class are not only subject to all the symptoms of 
the first and second, but frequently surgical operations are nec- 
essary to establish healthy relations between the digestive 

Deformities of the jaws and teeth are not uncommon. 
Macaulay portrays a vivid picture of such a state in Charles V 
of Spain. Among other physical deformities, he says, "At 
length a complication of maladies completed the ruin of all his 
faculties. His stomach failed, nor was this strange, for in him 
the malformation of the jaws, characteristic of his family, was 
so serious that he could not masticate his food, and he was in 
the habit of swallowing ollas and sweetmeats in the state in 
which they were set before him. While suffering from indiges- 
tion, he was attacked by ague. Every third day his convulsive 
tremblings, his dejection, his fits of wandering, seemed to indi- 
cate the approach of dissolution." 

Prof. Russell H. Chittenden 2 in his experiments in physio- 
logical economy in nutrition, has shown that excess of proteids 
means waste, "but of far greater importance is the unnecessary 
strain placed upon the body by this uncalled-for excess of food 
material which must be gotten rid of at the expense of energy 
that might better be conserved for more useful purposes." 

He has conclusively shown that body equilibrium can be 
maintained on half the daily intake of food. The brain worker 
and the muscle worker can maintain health, strength and vigor 
on a smaller amount of nitrogenous material than is usually 
consumed ; ' ' that an excess of food is in the long run detrimental 
to health, weakening rather than strengthening the body and 
defeating the very objects aimed at." This applies to people 
who have obtained their growth and not to children. 

Some neurotics and degenerates are very susceptible to auto- 
intoxication on account of unstable nervous systems. They 
either become easily constipated or toxic material accumulates 

Physiological Economy in Nutrition. 


in the intestines and as a result the system becomes slowly 
poisoned. Convulsions occur in both children and adults. 
Most, if not all, insane patients are constipated. While it would 
not be safe to say that the insanity was due to constipation, yet 
all are greatly benefited, and some slight forms are cured, by 
keeping the bowels free from microbic infection. 

Some of the best specialists claim the skin eliminates very 
little of the blood's poison. Under ordinary circumstances the 
skin excretes water, salts in small quantities, carbonic acid, and 
in some volatile fatty acids. As age advances and the elim- 
inating organs lose their activity, the bowels and kidneys fail 
to eliminate all the decomposed material. When these organs 
become diseased, the skin and lungs assist in carrying off the 
poisons or their products. The skin especially is important in 
keeping the system in a healthy condition, free from poisons. 

What the laity understand as "spring fever" is but the re- 
adjustment of the eliminating organs from winter to spring. 
People in the senile stages feel better in warm climates than in 
cold, hence the custom of moving to warm climates in winter. 

During pregnancy, poisons are formed in the mother and 
fetus which circulate in the maternal and fetal blood. Upon the 
mother is thrown the burden of eliminating by the kidneys, liver, 
intestines, skin and lungs the bulk of the poison formed within 
the two organisms. When these poisons are retained auto- 
intoxication is produced which varies in degree from heighten- 
ing the arterial tension, headache, gastric disturbance, and lassi- 
tude to convulsive seizures as in puerperal eclampsia. Intersti- 
tial gingivitis is always present to a more or less marked degree. 
The urine under these circumstances usually contains albumin. 
That errors of diet often induce puerperal eclampsia, there is 
no doubt. Pregnancy frequently advances normally until some 
such improper food as lobster, fish, pork, pie, strawberries, etc., 
is eaten ravenously, when, as the result of the entrance into the 
blood of imperfectly digested products or intestinal poisons, 
eclampsia follows. The presence of these toxins in the blood 
induces structural alterations in the renal epithelia and as a 
consequence renal debris, tube casts, are present in the urine 
along with albumin. If the patient lives the morbid changes are, 


for the most part, temporary, for they disappear on cessation 
of the pregnancy. We are familiar with the dropsical legs of 
women seen near the end of pregnancy, but it occasionally hap- 
pens that there is in addition to the autointoxication from intes- 
tines and kidneys, a hepatic toxemia, as well. 

An abnormal degree of urinary acidity extending over a 
period of nine months accounts for many of the neuralgias, 
toothaches, destruction of teeth by erosion, decay of the teeth 
and wasting of the alveolar process, skin diseases, and many 
other lesions so common in pregnancy which cease to trouble 
after birth of the child. Mental strain due to overwork, grief, 
shock, etc., check the secretions, causing an abnormal degree of 
urinary acidity which eventually results in diabetes, Bright 's 
disease and arterial degeneration. There are many other lesions 
traceable to or influenced by a high acidity of the system. 

The liver becomes enlarged and tender, the patient slightly 
icteric, the stools pale, fluid appears in the abdominal cavity, and 
there are albumin and bile in the urine. It is not until the preg- 
nancy has been brought to a natural or an artificial termination 
that the symptoms and physical signs disappear. In such a case 
the liver has failed to arrest and destroy the intestinal poisons 
as they pass through it and the result is that owing to their 
excess in the blood and inability on the part of the kidneys to 
eliminate them the patient is poisoned by the products within 
her own body. 3 

One accustomed to the odor of the skin and lungs and to an 
examination of the mouth in which there is interstitial gingivitis, 
can readily detect intestinal fermentation and kidney irregular- 
ity. Many times I have detected a tendency to kidney lesions 
or the lesion itself, in this manner, as was confirmed by subse- 
quent urinalysis. 

Autointoxication in disease is familiar to us all. That the 
blood is charged with effete matter or poison, due to autointox- 
ication, is abundantly proven. Owing to a swollen mucosa or 
other obstruction, ordinary nose breathing furnishes an insuffi- 
cient supply of oxygen. More air is necessary, hence the uncon- 

Autointoxication in Disease. 


scions opening of the month. A larger volume of air by nose 
and mouth is therefore taken into the lungs. Most people at the 
senile stage do this, most noticeably, however, at night. 

The poisonous products of the intestinal canal not expelled 
from the bowels are absorbed and carried by the portal system 
to the liver. If toxic material is sufficiently modified by the liver, 
it will be carried back and emptied into the bowel along with the 
bile. If, owing to some mechanical obstruction, as catarrhal 
swelling, gall stones or thickening of bile, the normal function 
of the liver should be interfered with, hepatic insufficiency re- 
sults. Any derangement of the bile or liver cells which inter- 
feres with the proper function of rendering harmful substances 
innocuous would cause abnormal and poisonous products to be 
carried in the blood. 

The great outlet for poisons which the liver fails to eliminate 
are the emunctories, chief of which are the kidneys. If there 
be too much work in this direction, the eliminating function is 
soon lost. The toxic material accumulates and results in renal 
inflammation and albuminuria. When this has taken place the 
blood becomes charged with poisons, the heart and arteries 
undergo degenerative changes with cardiac hypertrophy and 
arteriosclerosis together with the consequent cardio-vascular 
diseases, insufficient blood supply to various vital organs, nerv- 
ous disorders, Bright 's disease, diabetes, rheumatism, gout, uric 
acid diathesis, skin eruptions and asthma result. Before these 
diseases have become of sufficient importance to be observed by 
the physician, interstitial gingivitis has obtained full sway. In 
all the above mentioned diseases interstitial gingivitis is most 

The effects of autointoxication on the system are to reduce 
its vitality or to destroy the tonicity of the nervous system, the 
result of which, end organs of the body, the kidney, the brain, 
the eye, the dental pulp and the alveolar process first become 
diseased. This disease is brought about by overstrain upon the 
peripheral nerves, change in chemical structure of their blood 
cells, irritations upon the coats of the blood vessels and a gen- 
eral weakening of the part. The organ first involved depends 


upon its anatomy, its structure, its function, its weakness, local- 
ity, power of recuperation, etc. 

The poisons circulating in the blood, due to autointoxication, 
collect in the peripheral blood vessels of the alveolar process, 
change the character of the red blood cells and prevent nourish- 
ment from going to the parts. 

A low vitality of the structure is produced. Irritation of the 
vessel walls is set up and absorption of the process results. Peo- 
ple in advanced years in comparative good health (not ill), who 
are attending to their various affairs each day but who do not 
throw off the poisons of the body as readily as they did formerly, 
have an absorption of the alveolar process beginning at the gin- 
gival border and slowly extending toward the apical end of the 
root or roots of the teeth. The severity of this interstitial gin- 
givitis will depend upon the vitality of the patient and the degree 
of poisons circulating in the blood. How much more severe, 
therefore, must be the absorption when disease of one or more 
organs of the body occurs, especially the eliminating organs. 

It has been shown that poisons originating anywhere in the 
alimentary canal have been found in the urine, that poisons en- 
tering the system subcutaneously have been found in the urine. 
Some of these poisons are modified in form and intensity of 
action, while others remain in their original state. It has been 
a mooted question just how these poisons are excreted by organs 
in which they are not formed but a sensible conclusion must be 
that they enter the blood and are conveyed by it throughout the 
system and partly eliminated by the kidney. 

In a logical understanding of autointoxication and its treat- 
ment an examination of the urine should be made in order to 
ascertain the extent of poisons circulating in the blood. 



That changes in the character of the blood composition take 
place from week to week is known to every physician. These 
changes may be due to systemic derangement or to the character 
of the food, and are often so great as to affect the character of 
the tissues of the body, especially the alveolar process. We 
have at present no definite method of testing, from time to time, 
the chemical constituents of the blood. The best and only method 
of obtaining an approximate knowledge is by an examination of 
the urine. For many years I have made a special study of the 
constitutional condition. 

The examination of the urine is the only means at hand of 
ascertaining the general condition of the system underlying 
interstitial gingivitis. Two factors are of considerable moment, 
namely, an excess or diminished urinary acidity and indican. I 
wish to report three hundred and ninety-four examinations. 
The patients are from twenty-seven to sixty-seven years of age. 
All had interstitial gingivitis in its most aggravated form with 
loose teeth in varying numbers. Thirty-two had lost teeth as a 
result of the disease. Fourteen had pyorrhoea alveolaris that 
could be observed by the naked eye. Twenty-four hours' urine 
was obtained. A part or all was sent to the Columbus Medical 
Laboratory for examination. In tabulating the reports, the fol- 
lowing results were obtained : Specific gravity taken in the first 
fifty only, showed two had 1,005; two, 1,006; two, 1,008; two, 
1,009; one, 1,010; one, 1,011; one, 1,012; two, 1,013; six, 1,014; 
one, 1,015; five, 1,016; two, 1,017; one, 1,018; five, 1,020; three, 
1,023; one, 1,024; three, 1,025; one, 1,026; two, 1,027; one, 1,028; 
two, 1,029 ; one, 1,031. There were granular casts in six reports ; 
hyaline casts in twelve ; cylindroid in twenty-two. 

The degree of acidity was obtained by taking 10 c.c. of urine 
specimen, measured in the graduate glass, then placed in the 
small glass ; four drops of phenolphtalein were added; then drop 
by drop NaOH (1-10 normal sodium hydrate) until a slight pink- 


ish color was produced. Having noted on paper the number of 
c.c. of the NaOH in the burette before and after the pink color 
was obtained, the number of c.c. displaced multiplied by 10 (in 
order to find the number of c.c. NaOH necessary to neutralize 
100 c.c. urine) equaled the degree of acidity. Each step in this 
operation must be carefully performed, each instrument must 
be kept perfectly clean in order to get good results. 

The results showed two had 4 degrees ; two, 6 ; one, 7 ; two, 8 ; 
nine, 10; three, 11; seven, 12; one, 13; eighteen, 14; five, 15; 
twenty, 16 ; five, 17 ; two, 17.5 ; fifteen, 18 ; twenty-seven, 20 ; four, 
21 ; thirteen, 22 ; sis, 23 ; fourteen, 24 ; seven, 25 ; fifteen, 26 ; one, 
27; seventeen, 28; one, 29; thirty, 30; two, 31; nineteen, 32; six- 
teen, 34 ; six, 35 ; twenty-seven, 36 ; five, 37 ; eleven, 38 ; two, 39 ; 
twenty-two, 40; two, 41; eight, 42; nine, 44; two, 45; ten, 46; 
two, 47 ; seven, 48 ; one, 49 ; eight, 50 ; one, 51 ; six, 52 ; two, 53 ; 
one, 54 ; one, 55 ; fifteen, 56 ; one, 57 ; five, 58 ; two, 59 ; seven, 60 ; 
six, 62 ; three, 63 ; four, 64 ; three, 66 ; two, 68 ; four, 70 ; three, 72 ; 
two, 74; five, 75; one, 76; one, 78; one, 79; one, 80; one, 83; one, 
84 ; two, 100 ; three, 104 ; one, 105 ; one, 108 ; one, 110 ; one, 113 ; 
one, 120 ; three, alkaline ; two, neutral. The urea showed two had 
.3 per cent; one, .5; two, .6; two, .7; two, .9; two, 1; one, 1.1; 
two, 1.3; one, 1.4; four, 1.5; six, 1.6; one, 1.7; three, 1.8; one, 1.9; 
one, 2; three, 2.1; three, 2.2; two, 2.4; six, 2.5; two, 2.6; one, 3; 
one, 3.1; one, 7.1. Albumin was found in four cases; blood in 
six ; leucocytes in forty-five ; epithelial cells in forty-six ; uric acid 
crystals in two ; urates in five ; oxalates in fifteen. Of the three 
hundred and ninety-four examinations, three hundred and 
twenty showed indican to a greater or lesser extent. Seventy- 
four were normal in this respect. 

To make a more complete study of each individual case, the 
following table has been prepared : 

Specific Casts. 

Gravity. Granular. Hyaline. Cylindroid. 

23 * 

20 1 1 1 

8 1 

6 11 



29 1 1 1 




Per cent. 






















lar. Hyaline. 


d. Degree. 

Per cent. 







































































degree not 






















degree not 








degree not 































































Qualitative Examination. 

Physical condition : Present 30 

Clear 17 Absent 29 

Cloudy 33 Albumin : 



Reaction : 

Present, trace .... 









. . . .None 



.... None 




. . . .None 



Blood : 












Mucin : 

Microscopical Examination. 

Casts : 





Epithelial cells. . . . 




Crystals : 



Uric acid 


Cylindroids .. 










Leucocytes . . 




The relation of acid autointoxication and mouth acidity is 
very intimate. The acids taken into the body and those pro- 
duced by chemical changes within, such as hydrochloric, lactic, 
acetic, diacetic, oxybutyria, uric, and other acids circulate in the 
system in the form of salts so that the blood maintains at all 
times essentially a neutral reaction. If the acid ions in the blood 
at any time overbalance the metallic ions so that there is a con- 
siderable number of H ions present, an excretion of acid takes 
place and passes out through the kidneys, lungs, skin, and 
mucous membrane, especially of the mouth. If the kidneys do not 
carry off the surplus acidity, a greater strain is put upon the 
lungs, skin and mucous membranes of the mouth. The alveolar 
process and gums, being doubly transitory, as well as end organs, 
contain excretive and secretive glands. The gums are the first 
structure of the body which indicate systemic defects partic- 
ularly noticeable in mercurial, lead, and brass poisoning, scurvy, 
etc. The mucous glands normally excrete acid fluid, while the 
salivary glands secrete alkaline fluid. It not rarely happens, 
however, that the kidneys fail in their function and the system 
becomes so saturated with acid that the salivary glands continue 
to cause destruction of the teeth. 

Friction of the lips, teeth, and foreign bodies assist greatly in 
tooth destruction. Teeth softened by faulty nutrition and acid 


states are easily destroyed by acids and friction. 

In an examination of the urine of diabetics, tabetics and 
paretic dements, I have the following statistics : 

1. Urinalysis of Diabetic Patients. — Urinalysis by the Co- 
lumbian Medical Laboratories of three hundred and ninety-four 
diabetics showed specific gravity, one 1.003, one 1.005, one 1.007, 
one 1.010, one 1.011, eight 1.012, one 1.013, six 1.014, six 1.015, 
four 1.016, five 1.017, seven 1.018, six 1.019, seven 1.020, five 
1.021, thirteen 1.022, fifteen 1.023, ten 1.021, twenty 1.025, thir- 
teen 1.026, thirteen 1.027, eighteen 1.028, nineteen 1.029, twenty- 
five 1.030, twelve 1.031, fifteen 1.032, twenty-eight 1.033, sixteen 
1.031, twenty 1.035, seventeen 1.036, eighteen 1.037, nine 1.038, 
twelve 1.039, ten 1.010, eight 1.011, eight 1.012, two 1.013, seven 
1.011, two 1.015, two 1.016. 

Percentage of Sugar. — Twelve had 0.1 per cent, eighteen 0.2, 
three 0.3, eleven 0.1, seven 0.5, seven 0.6, one 0.7, four 0.8, eight 
0.9, ten 1, one 1.1, eight 1.2, seventeen 1.3, six 1.1, one 1.5, thir- 
teen 1.6, seven 1.7, four 1.8, one 1.9, five 2, three 2.1, six 2.2, 
three 2.3, seven 2.4, three 2.5, five 2.6, one 2.7, three 2.8, three 
2.9, four 3, one 3.1, five 3.2, six 3.3, one 3.1, two 3.5, ten 3.6, five 
3.7, five 3.8, fifteen 1, four 1.1, five 1.2, two 1.3, two 1.1, three 4.5, 
eight 4.6, four 4.7, five 4.8, five 4.9, five 5, two 5.2, ten 5.3, five 5.4, 
one 5.5, nine 5.6, seven 5.7, five 5.8, one 5.9, nine 6, five 6.1, ten 
6.2, ten 6.4, one 6.5, five 6.6, one 6.7, three 6.8, five 6.9, three 7, 
one 7.1, two 7.2, two 7.3, two 7.4, one 7.6, one 7.7, three 7.8, one 
7.9, one 8, one 8.2, one 8.5, one 8.7, one 9, one 9.1. 

Degree of Acidity. — Two passed 4 degrees, two 6, one 7, two 
8, six 10, five 12, sixteen 14, one 15, fifteen 16, one 17, thirteen 
18, twenty 20, one 21, twelve 22, one 23, ten 24, two 25, fourteen 
26, sixteen 28, one 29, twenty-one 30, seventeen 32, thirteen 34, 
four 35, twenty 36, two 37, eleven 38, two 39, thirteen 40, one 41, 
eight 42, seven 44, two 45, eight 46, two 47, five 48, five 50, five 52, 
one 54, twelve 56, one 57, four 58, five 60, one 62, one 63, three 
64, two 66, two 68, two 70, three 72, one 74, one 75, one 100, two 
104, one 120, one alkaline, two neutral. 

Acetone. — Of this number of cases only nineteen were exam- 
ined for acetone. In eleven, acetone was present, in eight absent. 
Thirty-two were examined for diacetic acid; in six it was pres- 


ent and in twenty-six absent. Twenty-four were examined for 
oxybutyria ; in all it was negative. 

2. Urinalysis of Tabetic Patients. — Degree of acidity in 
thirty-five was as follows : One passed 5 degrees, one 6, one 7, 
three 9, two 10, one 11, one 14, one 17, two 19, two 20, one 22, one 
46, one 48, one 49, one 50, one 56, one 62, one 73, two 76, one 78, 
one 81, one 82, one 84, one 97, one 99, one 112, four alkaline. 
Those patients having the alkaline urine had marked erosion of 
the teeth showing that at some time there had been a high degree 
of acidity. Cystitis caused the urine to become alkaline. All 
showed indican to a greater or less extent. 

3. Urinalysis of Paretic Patients. — Degree of acidity: 
There were twenty-one males, four females. Three passed 5 
degrees, one 7, three 8, two 9, one 10, one 11, one 12, one 13, one 
15, two 16, one 17, one 22, one 28, one 34, one 38, one 39, one 44, 
one 51, one 52, one 70. These patients were in a quiet state. If 
the urine could have been examined after excitement or an ex- 
plosion the degree of acidity would have been greater. 

4. Urinalysis of Private Patients. — Degree of acidity: I 
examined one hundred and twenty-nine. Three were also sent to 
me by Dr. J. F. Keef e of Chicago, making in all one hundred and 
thirty-two. They were from eleven to eighty-four years of age. 
All showed erosion and abrasion to a greater or less extent. 
Three passed 2 degrees, three 8, two 10, two 11, seven 12, two 
14, two 15, five 16, six 18, two 19, eight 20, five 22, five 24, six 26, 
four 28, two 29, six 30, two 31, four 32, two 33, three 34, nine 36, 
two 38, two 40, two 44, five 46, one 47, two 48, two 50, five 52 ; five 
54, four 56, one 58, three 60, two 62, five 70, one 90, one 127, one 
132, only four or 3.8 per cent had uric acid. I quote here from a 
previous paper, "Interstitial Gingivitis Due to Autointoxica- 
tion," my first fifty patients' degree of acidity, one had 11 de- 
grees, two 12, one 14, two 15, one 16, two 17.5, four 20, one 22, one 
24, five 30, seven 36, two 40, two 44, one 46, two 56, one 58, one 59, 
one 60, two 62 ; 3 per cent had uric acid, all had indican. 

The acidity of a single specimen of urine will vary like the 
specific gravity within large units, corresponding to the amounts 
of acid entering the blood from various sources. The normal 
degree of acidity of the urine is from 30 to 40 degrees. A low 


acidity may arise from several factors : 1. A large excretion of 
water, as in nervous states, diabetes insipidus, etc. 2. A diet con- 
taining a large quantity of salts of the vegetable acids. 3. A cor- 
responding deficiency of meat which yields acid salts. 4. A defi- 
cient power of the kidney to excrete acid. 5. Excessive elimina- 
tion of acid by other emunctories. In patients in whom the 
degree of acidity exceeds 40°, there is excessively imperfect oxi- 
dation which, irrespective of the types of acid, underlies, as is 
now pretty generally recognized, severe constitutional stress 
allied to that of diabetic acidosis. 

The quantity of urine passed in twenty-four hours influences 
the degree of acidity. Thus, if more than 40 ounces (about the 
normal amount) be passed, the degree of acidity with the same 
total amount of acid would be low as compared with less than 
40 ounces. 

On application of the phenolphtalein, if the urine specimen 
turns pink, it is alkaline, therefore no degree of acidity can be 
obtained. Litmus paper is applied to the gums and lips to ascer- 
tain if the mucus be acid. Acid mucus was found in every case 
tested. The circle of evidence, therefore, is complete. 

Few adult persons have not had an excess of acidity at some 
period. Complete oxidation is essential to a normal condition. 
The organs and tissues of the body act as best they can to bring 
about this condition. In some systems, the liver has all it can do 
to care for the waste products of the tissues themselves. That 
the salts of fruit acids may be converted into alkaline substances 
in the system is true. The liver and tissues become overworked. 
The fruit habit (especially grape fruit) so generally indulged in 
to excess in America is producing havoc with the alveolar proc- 
ess, gums and teeth. 

One case is sufficient illustration of the many requiring treat- 
ment. A twenty-seven-year-old woman had her teeth and mouth 
put in good condition in January, 1907. February 16 she re- 
turned with what she thought a cavity at the cervical margin of 
the left superior cuspid. Upon examination, I found the gums 
inflamed and receding, not only at that particular location but 
about all the teeth. Previous to this, the gums and mucous mem- 
brane were in fairly good condition. Litmus test showed the 


mucus to be very acid. There was no cavity, only sensitive ex- 
posed dentine. Much gas was passing from the stomach. Upon 
interrogation in regard to her food she informed me she had 
been eating grape fruit every morning for three weeks. Urin- 
alysis of a twenty-four-hour specimen showed the degree of 
acidity to be fourteen. Sixteen degrees were retained in the 
system. The recession of the gums and the sensitive dentine 
were due to the acid retention. The skin, lungs, and mucous 
membranes try to dispose of the surplus. If these structures are 
unable to do so, they are expelled as gas, vomit, or fermentative 
stools. That the acid excess of the system does pass through the 
mucous and salivary glands of the mouth to produce destruction 
of tissue, has already been demonstrated. With these illustra- 
tions of tissue in the mouth the question arises how far does this 
acidity affect other tissues and diseases of the body? For want 
of time, merely a few urinalyses in diseases were made. 

Disease. Degree of Urinary Acidity. 

Arthritis (rheumatoid) One 70. 

Backache (severe) One 10 ; one 25 ; two 30 ; one 35 

one 36; .one 40; one 50; one 79 
one 82; one 87; one 90; one 95 
two 100 ; two 110 ; one 120. 

Bronchitis One 56 ; one 58 ; one 60 ; one 61 

one 67 ; one 120. 

Constipation One 25. 

Ooryza (acute), children 3 to 13 yrs.Onel2; two 13; one 14; one 15 

one 16; one 17; one 20; one 22 
one 26; one 27; one 30; one 36 
one 46; one 47; one 50; one 56 
three 58; one 70; one 72; one 90 

Cystitis (acute) One 50. 

Diphtheria One 28. 

Dipsomania One 44. 

Eczema (hands) One 50 ; one 80. 

Enlarged prostate One 100. 

Enterocolitis (chronic) One 35 ; one 80 ; one 110 ; one 112 

Exophthalmic goiter (puberty stress) One 54. 

Fibrillae tremor One 21. 

Gastric hyperchloridice One 60. 

Gonorrhea One 120. 

Grippe Two 25 ; one 40 ; one 50 ; one 60 

one 75 ; one 76 ; one 80 ; one 82 
one 88; one 90; one 94; one 97 
one 110.. 

Hypertrophic rhinitis (acute) One 21; one 25; one 113. 

one 100 

; one 112. 

one 24; 

one 25 ; 



one 46. 

one 26 ; 

one 27; 



one 12; 

one 14; 



one 29; 

one 30; 



one 60; 

one 62; 



one 82 ; 

one 84. 

one 84. 

one 15; 

one 18; 



one 24; 

one 27 ; 



one 57; 

one 61; 



one 80. 

one 108 

one 132 


Hypertrophic rhinitis (chronic ) One 32; one 57; one 90. 

Laryngitis (chronic) One 65 ; one 85. 

Middle ear, inflammation of One 25 ; one 32; one 90. 

Middle ear, chronic suppurative in- 
flammation of One 90. 

Meniere's disease One 65. 

Migraine One 40. 

Myocarditis (chronic) One 80; 

Neuralgia following grip One 20; one 24; 

one 40 ; 

Pneumonia One 18 ; 

Pregnancy One 10 ; 

one 18; 

one 57 ; 

one 67 ; 

one 82 ; 
Rheumatism and gout One 14; 

one 20; 

one 52; 

one 70. 
Rheumatism and heart trouble. 8 

years of age One 40. 

Scarlet Fever One 33 ; 

Sciatica One 55 ; 

Sphenoid sinus, inflammation of . . . . One 57. 

Sunstroke One 20. 

Tired feeling One 25 ; one 40. 

Tonsilitis (ulcerating) One 10 ; one 12 ; one 14 ; one 20 ; 

one 27 ; one 48 ; one 72. 
Tuberculosis One 16 ; one 20 ; one 21 ; one 36 

one 44; one 52; one 56; one 78 

one 81 ; one 88 ; one 102 ; one 108 

one 115 ; one 142. 

Tuberculous hip disease One 80. 

Tvphoid Fever One 76 ; one 88 ; one 90 ; one 109 ; 

one 120. 
Urticaria One 47. 

On comparing the office patients with those of other special- 
ists and patients ill at home or in a hospital, it is found that the 
degree of acidity does not vary to any great extent. A constant 
abnormal degree of urinary acidity, in an individual attending 
to his affairs, means that sooner or later an organ or structure 
is bound to give way. This is particularly true at the senile 
period of stress (about sixty) when the arteries degenerate. The 
victim of an abnormal degree of acidity is more subject to dis- 
ease than one with normal acidity. Study of the effects of a high 
degree of acidity in an otherwise normal individual whose teeth 


and alveolar process are being destroyed has exceedingly inter- 
esting results. 

Lessened blood alkalinity affects the whole alveolar process 
by setting up an irritation and inflammation of the coats of its 
arterioles and in the tooth pulp, producing endarteritis oblit- 
erans, arteriosclerosis, and nerve-end degeneration. I have dem- 
onstrated those diseases many times. Disease of the terminal 
nerves and arteries causes absorption of the bone. The inflam- 
matory process has been termed interstitial gingivitis ; the bone 
absorption, osteomalacia, or senile absorption, although it may 
occur early in life. 

May not osteomalacia in other parts of the body be due to the 
same cause? 

Cylindruria 1 is not necessarily associated with definite path- 
ologic alterations of the renal parenchyma. This statement 
should likewise be accepted as to the occurrence of purely hyaline 
casts and their presence in small numbers. A few renal epithe- 
lial cells may be found at the same time occurring either in the 
urine or adhering to the casts, but never presenting an atrophic 
or otherwise altered appearance in the absence of definite renal 
lesions. The presence of compound hyaline and coarsely gran- 
ular casts, as well as of waxy and amyloid casts, on the other 
hand, may be regarded as indicating definite changes in struc- 
ture, so that as far as diagnosis is concerned microscopic exam- 
ination of the urine furnishes information of more value than the 
simple demonstration of albumin. 

Hyaline casts are more frequently seen — reference is here 
made only to the purely hyaline or, at least, but faintly granular 
form — and are found in all conditions in which albuminuria 
occurs. When present in only small numbers, and particularly 
when occurring but temporarily in the urine, it may be assumed, 
in the absence of other symptoms pointing to renal disease, that 
there is a mild circulatory disturbance of the kidneys. 

The significance of blood and epithelial cells imbedded on 
hyaline casts is the same as the significance of blood and epithe- 
lial casts ; both are pathologic and indicate nephritis. 

Clinical Diagnosis, p. 620. 


Fine granular and hyaline casts often occur from auto-toxic 
strains on congenitally insufficient kidney in arthritic and allied 

The presence of albumin in these cases was exceptional, it 
being found in but four cases. This would show that in none of 
these cases had the disease become very marked. When present 
it does not in itself indicate grave disorder, since albumin may 
be due to many conditions of the renal tract. It is of interest 
to us since disturbance of circulation may bring about albu- 
minuria without inducing structural change in the kidneys. 
Purdy says: "Circulatory disturbances, in order to induce 
albuminuria, must include the renal vessels. In nature they 
must consist of acceleration of the arterial current or slowing 
of the venous current, in either case resulting in increased blood 
pressure. Again, in some derangements of the nervous system 
which interfere with the vasomotor nerve regulation of the renal 
vessels, temporary albuminuria is not an uncommon result." 
Albuminuria is present in auto-toxic neurasthenia, epilepsy, 
paretic dementia, and the renal crises of locomotor ataxia. 

The specific gravity ranges from 1.005 to 1.031. The normal 
specific gravity ranges from 1.015 to 1.025. The difference de- 
pends upon the amount of solids and fluids present, increasing 
as the solids increase, decreasing as the amount of fluids increase. 
Specific gravity is hence an index in a general way of metabolic 
change. The low degree of acidity would indicate that a certain 
amount of acid was circulating throughout the system. 

Indicanuria denotes the presence in the urine of potassium 
indoxyl sulphate formed by metabolism of indol absorbed from 
the intestines. It is supposed to be due to three sources : First, 
to intestinal putrefaction of nitrogenous substances; second, to 
suppuration in some part of the body; and third, to the forma- 
tion of indol in the cells of the body-tissues. The fact that 
indican is found in the urine is a sufficient indication that this 
poison has circulated in the blood throughout the entire system 
and has been returned to the kidneys to be expelled. I have dem- 
onstrated many times that indicanuria and neurasthenia are in 
some way related. Reducing the intestinal putrefaction by the 
use of intestinal antiseptics, the neurasthenic condition of the 


patient is often relieved. The toxic effect of acidosis and indican 
upon local tissues, especially upon terminal and transitory 
structure, is very marked. Their injurious effects consist of 
irritation of the coats of the blood-vessels and changing the 
chemical quality of the red blood cells. The salivary glands, the 
mucous glands, the alveolar process, and the dental pulp are the 
first structures to become involved. 

Indicanuria is one of the great sources of autointoxication. 
The toxins of indican permeate all the structures of the body, 
being carried by the blood circulation. While acidosis and in- 
dicanuria may go hand in hand, the quantity of indican depends 
to a certain extent upon the acidosis relative to the amount 
formed in the intestines. Thus, upon reducing a high degree of 
urinary acidity to normal or below, the indican will be increased, 
owing to the abnormal bacterial activity in producing putrefac- 
tion. These germs seem to thrive better in alkaline than in acid 

An accumulation of indican in the organism will often cause 
febrile disturbances, lassitude and gastrointestinal irritation — 
depending, of course, upon the severity of the attack. The 
effect of indican is not unlike that of poisonous drugs such as 
mercury, lead, phosphorus, bromine, quinine, etc., which pro- 
duce poisonous symptoms in some individuals. In others there 
are apparently no ill effects. It must, therefore, not be over- 
looked that in all persons with persistent indicanuria the poison 
is continuously absorbed from the intestines into the circulation 
for months and years, and that in many persons it will not mani- 
fest itself until the periods of stress at forty-five and again at 
sixty years of age. Metchnikoff, in considering the phenomena 
of old age, concludes that autointoxication due to intestinal 
putrefaction is one of the most important causes of premature 
senility, in that it causes arteriosclerosis. The accumulation of 
these toxins in terminal organs, such as the pulp and alveolar 
process, is as disastrous as the accumulation of any of the poison- 
ous drugs. Arteriosclerosis is one of the common diseases found 
in the alveolar process and in the pulp, which is a positive 
proof of its systemic origin. 

To obtain the amount of indican in a given specimen, take 


5 ccm. of urine; pour it into a test-tube; add 5 ccm. of hydro- 
chloric acid, and shake thoroughly. Let the mixture stand for a 
few moments. Add 10 drops of hydrogen dioxide, shake thor- 
oughly, and let it stand for a few moments ; then add 1 ccm. of 
chloroform, shake thoroughly again, and let it stand. If indican 
be present, chloroform will absorb it, turn blue, and settle to the 
bottom of the tube ; if there be no indican, the chloroform will 
remain colorless. 

The toxins in the blood which accompany acidosis and indi- 
canuria are carried to all structures of the body. All structures 
of the body, however, are not alike. Some, especially those that 
are active and are needed for the welfare of the body, under the 
law of economy of growth or use and disuse of structures, can 
take care of the toxins and return the blood to be cleansed of its 
impurities. Other structures which are of little use, and are 
called terminal organs and transitory structures, such as the 
dental pulp and the alveolar process, cannot dispose of the 
blood so readily. The result of this is an accumulation of tox- 
ins, and disease follows. Other terminal organs that can stand 
the strain a little better, but are sure to succumb later if the 
toxins continue to be present; in the blood, are the kidneys, the 
heart, the liver, the eye and the brain. 

I wish to call the attention of the profession to the fact that 
early symptoms and systemic disorders may be recognized, and 
prophylactic means may be adopted to ward off future trouble. 
Heart-pressure, endarteritis obliterans, arteriosclerosis and 
dilated arteries are easily demonstrable in the pulp and in the 
alveolar process by early symptoms of acidosis and indicanuria. 
It will be seen, then, that acidosis and indicanuria are factors 
which cannot be overlooked. 

Critical examination of tables must convince a careful ob- 
server that in every examination two conditions are present; 
first, autointoxication due to intestinal fermentations and faulty 
elimination as represented by the indican and an abnormal uri- 
nary acidity degree ; second, kidney over-strain and renal insuf- 
ficiency due to hepatic insufficiency. When the liver fails to de- 
stroy the poisonous materials and the bowels to eliminate the 
toxins, over-strain of the kidnevs causes the blood to become 


overcharged with toxins and acidity, the heart and arteries 
undergo degenerative changes, and cardiac hypertrophy and 
cardio-vascular diseases, with insufficient blood supply, result. 

It may be possible that in the near future other poisons than 
those already mentioned will be found in the urine, which may 
produce toxic effects on the alveolar process. Since this chap- 
ter was written, the following appears in the Journal of the 
American Medical Association: "A few unique anomalies of 
metabolism, notably alkaptonuria and cystinuria, have attracted 
attention quite as much because of the interpretation which they 
lend to the normal disintegration of protein in the body as on 
account of the pathologic features involved. From the fact that 
certain diamirs, cadaverin and putrescin, characteristic of the 
putrefaction of proteins, frequently are found in conjunction 
with cystin in the urine of patients, it has at times been assumed 
that there is an essential connection in cystinuria between ali- 
mentary putrefactive changes and the output of characteristic 
abnormal excretory products. Cystinuria, however, has been re- 
garded of late rather as an abnormality of protein metabolism 
in which the amino-acid cystin — a typical degradation product 
of albuminous substances — is not further broken down and oxi- 
dized as ordinarily. This view is strengthened by the simul- 
taneous finding of other amino-acids, leucin and tyrosin, in cer- 
tain cases. The latest novelty is the discovery of another amino- 
acid, lysin (diamino-caproic acid), in the urine of a patient with 
cystinuria. Since this compound is known to be the mother sub- 
stance of cadaverin, the intimate inter-relation of the various 
observed constituents is further emphasized. Taken together, 
the accumulated data strengthen the conception of cystinuria as 
a condition in which the usual progress of protein catabolism is 
profoundly inhibited. One by one the unused fragments are 
cropping out as new cases become available for study. ' ' 



Endarteritis obliterans and hypertrophy of the middle and 
outer coats of the arteries are physiologic processes concerned 
in the disappearance of blood vessels functional in the fetal 
state, but losing- such function after birth. Like all physiologic 
processes of the fetal type these become pathologic under ordi- 
nary conditions of post-natal life. For these reasons they again 
become physiologic in the involutional periods like the climac- 
teric and senility. In transitory structures, like the alveolar 
process, there is continual trembling between the physiologic 
and pathologic. Undue excitation of the structure brings on an 
intensity of the process which tends to become pathologic. As 
I demonstrated a decade ago, endarteritis obliterans and hyper- 
trophy of the middle and outer coats of the arteries play a large 
part in interstitial gingivitis. 

In consideration of this subject, the changes in the elasticity 
of the artery and vein walls and the permeability of the capil- 
lary walls will be discussed. 

The vessel walls are capable of great elasticity and bear the 
tension of the pressure of the blood without showing any condi- 
tion of being strained. This elastic function of the walls is con- 
trolled by the muscular coat, which changes the chemic energy 
of the blood stream into energy of elasticity and in this manner 
keeps the vessel walls in a normal elastic state. The changes 
that take place in the arterial walls of the aortic system are of 
more or less importance, since the normal elasticity of the 
artery walls, blood pressure regulation, and distribution are 
dependent upon the depth and intensity of these changes. 

When the vessel walls become diseased there may or may not 
be serious disturbance in the blood circulation. The acute and 
chronic contagions and infections, a general nutritional disturb- 
ance or poisons taken either internally or externally, and a high 


blood pressure tend to weaken the arterial walls so that their 
elastic tonicity, in some instances, is completely lost. 

This weakened elasticity is easily recognized by a distensile 
pulse and also registered by the sphygmomanometer. At the 
same time, arterial murmurs can be heard in the large arteries, 
especially the femoral, which are apparently a result of the 
rapid vascular changes characteristic of a high pulse. A pulse 
sometimes observed in retinal arteries can also be attributed to 
this source. 

In the conditions just mentioned there are no great circula- 
tory disturbances, but there is a tendency to change in the struc- 
ture of the arterial walls. As a result of this weakened state, the 
lumen expands and a larger amount of blood flows through the 
artery, but its rapidity is decreased. So with the alveolar pro- 
cess, the arteries and veins inclosed within bony walls have little 
or no expansion, hence the tissues become more susceptible to 
poisons and toxins circulating in the blood stream. The de- 
creased flow of the blood stream, in turn, causes new connective 
tissue to form in the intima of the artery, which thickens this 
outer coat, making it less elastic and reducing the pulse move- 

Any arteries of the body are liable to become involved, but 
more particularly those of the extremities and end organs. While 
puberty changes may produce a severe attack, the condition is 
more frequently noticed later in life — the later, the more pro- 
nounced. Men are more subject to the disease than women ow- 
ing to the fact that women eliminate much more freely than 
men, and because they are not often subjected to drug poisons. 
Coldness of the limbs, hard whip-cord arteries with no pulsa- 
tion, and, in extreme cases, gangrene of the extremities result. 
The disease begins in the intima and extends to the other coats 
of the artery. It may be found in all local inflammations of 
long standing, especially in the extremities, the alveolar process, 
and may occur in conditions of vasomotor ataxia, such as are 
present in Eaynaud's disease and allied conditions. Syphilis, 
tuberculosis, typhoid fever, scurvy, and the condition underlying 
arterio-capillary fibrotic kidney lesions act at times as predis- 
posing causes. Toxins and autotoxic products of retained waste 


may disturb physiologic balance, thus giving the pathologic 
phase of this disorder sway. 

Endarteritis is an inflammation of the internal coat of an 
artery or capillary, generally of chronic type. Its pathogeny is 
as follows: In direct contact with the blood streams is the 
endothelium (a layer of flattened cells) ; next is the tunica 
intima, composed of elastic fibers arranged longitudinally; next 
comes the middle coat, composed of muscular fibers arranged 
transversely. The outer coat consists of longitudinal connective 
tissue, which contains the vasa vasorum. In the capillaries, the 
intima lies in immediate contact with the surrounding tissues, or 
accompanied by a rudimentary adventitia. In other words, the 
walls of the capillaries consist of almost nothing but the intima. 
The capillaries have certain contractility; they contract or 
dilate without muscular fibers. The veins probably also have a 
certain amount of contraction and dilatation from irritability of 

Fig. 79. — Endarteritis Obliterans (Kaufmann). 

A, Adventitia. E, Elastic Tissue between Middle Coat and Intima. M, Muscular. 

J, Thickened Intima. 

the intima. Each coat of the arteries takes on a special type of 
inflammation. The causes of endarteritis are numerous. 

Inflammation of the intima of the blood vessels may be due 
to irritation from without or within. When it occurs from with- 
out, any local irritation will set up an inflammation which may 
extend to the outer coats of the capillaries. This produces a 
marked increase of blood. The vasa vasorum become swollen, 
the white blood corpuscles crowd into the terminal capillaries 
and migrate into the extra vascular space. Rapid proliferation 
of the round-cell elements takes place. The walls of the vessels 
become thickened. Owing to the projecting intervals of the 
intima, the caliber of the blood vessels diminishes (Fig. 79). 


Irritation occurring from within, results either from trophic 
changes in the system from direct irritation from toxaemias, or 
from both interdependently. Under these circumstances toxins 
may have an affinity for a certain organ, tissue or part, and pro- 
duce irritation in the capillaries in a distinct part of the body, 
or the capillaries through the entire body may become involved. 
Thus, in typhoid fever, the Peyer's gland in the intestine be- 
comes involved; in scarlet fever, the skin or kidney; in malaria, 
the liver and spleen; in Bright 's disease, the kidney; while in 
mercurial and lead poisoning and scurvy, the mucous membrane, 
and especially the gums, become diseased. In many of these con- 
ditions, however, before the tissue already irritated becomes 
involved, the nervous system has become affected. The nervous 
system may already have become affected from other causes. 
Thus, locomotor ataxia, traumatic injuries to the spine, paretic 
dementia, cerebral paralysis, neuroticism and degeneracy, and 
last, but not least, stomach neurasthenia. The poison in the 
blood, together with the diseased peripheral nerves, produce irri- 
tation and inflammation of the inner coat of the capillaries. If 
this irritation does not disappear soon after its inception, 
the inflammation tends to affect the other coats of the 
blood vessels. Under certain conditions, endarteritis may, 
however, never involve the other coats of the vessels. When 
irritation of the inner coat of the capillaries takes place, 
proliferation of the endothelium occurs. This inflammatory 
growth tends to obstruct the lumen of the vessel. The media 
may likewise become thickened by an increased connective tissue. 
The capillaries become obstructed, and finally obliterated. This 
finally impedes the circulation. Fig. 80 shows such a condition 
in the scurvy case, elsewhere illustrated. 

Irritation may be of less intensity but greater duration, as in 
cases of syphilis, tuberculosis, scurvy, mercurialism, plumbism 
(lead poisoning), etc, and the results are then slowly effected. 
Proliferation of sub-endothelial connective tissue gradually 
increases until it reaches its limit (endarteritis obliterans). This 
influence of the proliferation is exerted in addition to that of the 
round-cell infiltration about the structure. 



The recent studies of Hektoen 1 on meningeal tuberculosis 
demonstrate that tubercle bacilli may penetrate the unbroken 
endothelial layers of the vessel and stimulate marked prolifera- 
tion of the sub-endothelial connective tissue. An internal irri- 
tant, such as may be produced in the course of any infectious dis- 
ease or from suboxidation, probably acts upon the endothelium 
of the walls of the smaller blood vessels in such a way as to per- 
mit the escape through the walls first of serum, then of leuco- 

X 150. D. D. obj. Zeiss. 
Fig. 80. — Cross Section of Peridental Membrane, Showing Endarteritis 
Obliterans. Scurvy in Man. 
C, Cementum. D, Dentine. I, Peridental Membrane. U, Nerve Tissue. EO, Endar- 
teritis Obliterans. 

cytes, the latter infecting and surrounding the vessels. The effect 
of the chronic endarteritis is to check the blood supply to the gum 
tissue. Mercury, lead and other poisons circulating through the 
blood are forced to remain, hence discoloration of tissue along 
the gum margin. Interstitial gingivitis, resulting in a slow dis- 
turbance of nutrition, produces overgrowth of connective tissue. 
In all cases of chronic interstitial gingivitis, as shown in the illus- 
tration, are the blood vessels thus involved. 

American System of the Practice of Medi 


Among the predisposing influences which cause this disease 
are syphilis, tuberculosis, mercurialism, plumbism, brass poison- 
ing, lithaemia, nephritis, gout, rheumatism, alcoholism, scurvy, 
nervous diseases, pregnancy and old age. Under certain con- 
ditions of the system any and all diseases which tend to lower the 
vitality, producing anaemia, will assist in producing this disease. 
The direct cause may be resultant overstrain of the blood vessels. 

Owing to obliteration of the arterioles in the alveolar process 
stasis of blood must follow. The detritus from the alveolar proc- 
ess, therefore, must remain in the tissue and collect upon the 
roots of the teeth. 

Fig. 81. — Longitudinal Section of Gingival Border, Higher Magnification, Show- 
ing Eound-Cell Inflammation Extending to the Inner Coat of the Blood 
Vessel, and also Plasma — Mast Cells. 

Endarteritis obliterans and arteriosclerosis of the blood 
vessel walls in the alveolar process are always observed in con- 
nection with both local and constitutional diseases. 

No structure affords such a favorable opportunity for the 
study of endarteritis obliterans and arteriosclerosis as the alve- 
olar process in animals and human, since it can be obtained in 
quantities at all times and under all conditions. It may be pro- 
duced in healthy animals by the internal administration of drugs, 
metals and other poisons. 


My researches on this series of experiments were made upon 
humans, monkeys, and dogs. Decalcification of the alveolar proc- 

Fig. 82. — Arteriosclerosis in Tuberculous Monkeys. 

ess was made in weak acid solution and prepared for the micro- 
scope in the usual way. 

Fig. 83. — Transverse Section of Alveolar Process, Chronic Inflammation Ex- 
tending Throughout. Dog. 

On the administration of drugs, especially mercury or lead, 
to healthy young dogs, inflammation of the alveolar process with 



diseased arterial walls is seen at the end of a month or six weeks. 
Fig. 81 shows the commencement of the thickening of the intima 
in a dog. The coats of the arteries are well defined and the in- 
flammatory process has just begun. Examination of the alveo- 
lar process of animals or human beings suffering from disease, 
in which the eliminating organs are not throwing off effete mat- 

■Arteriosclerosis and Obliterans in Arteries op a Dog with 
Interstitial Gingivitis. 

ter, especially in syphilitic, tuberculous and scorbutic patients, 
easily reveals this morbid state. 

Fig. 82 is a poor illustration of the disease in pregnancy. If 
such patients are degenerates the process will be exaggerated. 

Fig. 83 illustrates endarteritis obliterans in the artery of a 
dog with interstitial gingivitis. 

Fig. 84 is from the alveolar process of a tuberculous monkey. 


«j , m 



' ,' ' v ' ? 



'v -'-i'l 

Fig. So. — Arteriosclerosis from Mercurial Poisoning. 


w ^ 



f ; 


^ 1 

Fig. 86. — Arteriosclerosis from Lead Poisoning. 



Fig. 85 illustrates the closing of three arteries from mercurial 

Fig. 86 shows endarteritis, obliterans with arteriosclerosis in 
interstitial gingivitis from lead poisoning. 

Fig. 87. — Arteriosclerosis and Obliterans prom Diabetes Mellitus. 

Fig. 87 shows arteriosclerosis and endarteritis obliterans in 
interstitial gingivitis from diabetes mellitus. 

Arteriosclerosis and Obliterans from a Syphilitic. 

Fig. 88 illustrates arteriosclerosis of three arteries in a syph- 

It will be seen from the illustrations that these pathologic 
conditions in the blood vessels of the alveolar process produce 
stasis of blood which cuts off the nutrition of the tissues. This, 
in turn, not only lowers the vitality of the parts, but together 
with local disturbances causes rapid destruction of the gums, 
peridental membrane and alveolar process. 



Since the brain presides over development of the tissues of 
the body through its trophic and vasomotor systems, it must be 
as fully developed and normal in construction as possible so that 
body tissues may develop normally. Pleasure, happiness and 
laughter aid digestion, while melancholia and grief may retard 
growth and function and produce tropho-neuroses. An unstable 
nervous system produces unstable tissues, i. e., either excessive 
or arrested. 

While the nervous system has other special functions, the one 
great object is that of regulating growth and repair. As Mari- 
nesco has shown, this function resides even in the neuron or 
nerve unit. Growth and repair are regulated through the trophic 
and vasomotor systems. In the domain of bone growth, trophic 
nerve anomalies were first observed. Brown-Sequard demon- 
strated anomalies in tabetic joints of sufferers from locomotor 
ataxia and later similar states were observed in the jaws. An- 
other allied neurosis, paretic dementia, presents similar trophic 
disturbances, as Kiernan pointed out thirty-five years ago. 2 

Among these tropho-neuroses is one characterized by loosen- 
ing and falling out of the teeth by alveolar resorption, gingival 
ulceration and perforation, with at times maxillary necrosis. 
This condition has long been recognized by alienists and neurol- 
ogists as causing that loss of the teeth which occurs in paretic 
dementia, locomotor ataxia and diabetes. This function of the 
trophic nerves, as I have elsewhere shown, has received but little 
attention from dentists, albeit its influence has been recognized 
in dental pathology in connection with the great neuroses in 
which gum disorder occurs, followed by a loosening of the teeth. 

Degeneration of the peripheral nerves due to interruption of 
the connection with the central nervous system was first shown 
by Nasse and Valentine in 1839. Not until 1850, however, was a 
thorough study made of nerve degeneration by Waller, the 
pathology of which is now known by his name. Wallerian degen- 
eration implies change in the terminal ends of the peripheral 
nerves after they have been cut, which consists in coagulation or 

'Journal of Nervous and Mental Diseases, 1878. 


breaking up of the myelin sheath, destruction of the axis cylin- 
der, the neurilemma with its nuclei remaining for some time pre- 
served. If a sensory nerve be cut through peripheral to the 
spinal ganglion complete degeneration ensues. 

Similar experiments showed that if the dorsal root of a spinal 
nerve be cut through at a point between the ganglion and the 
spinal cord the portion of the nerve attached to the ganglion did 
not undergo the typical degeneration, while the portion still con- 
nected with the cord showed the characteristic degeneration phe- 
nomena which could be traced throughout the whole course of its 
constituent fibers in the dorsal funiculi of the cord. The cells of 
the spinal ganglia have therefore been looked upon as trophic 
centers for the peripheral sensory nerves and their intramedul- 
lary continuations. 

Similar degenerations in the domain of the central nervous 
system likewise occur ; secondary descending degeneration of the 
pyramidal tract, established by Turck, and ascending secondary 
degeneration in the spinal cord after transverse lesion being 

Converting then, as Barker 3 remarks, the Wallerian doctrine 
into terms of the neuron concept, the following general law may 
be laid down: "Whenever it has suffered a solution of continu- 
ity, with severing of its connection with the cell body and den- 
trites of the neuron to which it belongs, the axon,, together with 
the myalin sheath covering it, undergoes in the part distal to the 
lesion acute and complete degeneration. This degeneration 
includes not only the main axon, but also its terminals, together 
with the collaterals and their terminals connected with it." 

Some investigations have shown that the slightest injuries to 
nerve cells or neura will give rise to easily demonstrable degen- 
erative lesions in other parts of the cell. The most significant 
instance is in lateral sclerosis, where the pyramidal motor cells 
of the cortex show no marked lesions, though the most distal por- 
tions of the nerve fibers arising from them have gradually 

In some peripheral nerve diseases, according to Strumpell, 

The Nervous System. Barker. 


the degeneration of the distal portion of the axones may be due 
to direct action of toxins exerting a deleterious influence upon 
the cell body or the whole neuron. In Wollenberg's opinion the 
primary type of disease of the sensory neura in tabes is of this 

As Sidney Kuh 4 has shown, in some of the toxic forms, as for 
instance in neuritis due to poisoning with lead and arsenic, the 
cells of the spinal cord as well as those of the spinal ganglia and 
brain may be diseased, and according to the neuron theory the 
toxic substances attack these cells before the nerve fiber itself is 
altered. Such an assumption explains why pronounced degen- 
eration of peripheral nerves may occur without causing any ap- 
preciable symptoms. Toxins and intoxications will produce the 
same results, especially in those nerves extending into and 
through the alveolar process. Pitres and Vaillard first showed 
that after typhoid fever, many nerve fibers are found degener- 
ated, in cases in which, during life, symptoms of neuritis were ab- 
sent. The same observers found like states in the nerves of those 
who had died from tuberculosis. Later observations have ex- 
tended these states to such diseases as diphtheria, syphilis, alco- 
holism, carcinoma, inanition, marasmus, arteriosclerosis and 
leprosy; in the so-called rheumatic neuritis of the facial nerve 
and to inflammation due to articular rheumatism, gout, puerperal 
infection, tuberculosis, etc. 

The method of cell poisoning has been observed in other 
intoxications. Certain groups of neura are more susceptible 
than others to a given toxication. The same group of nerve 
cells in two individuals may react very differently to similar 
doses of the same poison. Syphilitic toxin shows a decided 
preference for certain parts of the cerebral cortex, other areas 
being less affected. The nerve endings in all parts of the body 
are markedly involved, especially those in and about the teeth. 
Peripheral nerve degeneration results where the blood current 
or the nerves themselves are involved from faulty metabolism, 

Nerve lesions more readily result where nerves are confined 
within restricted walls of transitory structures where the pulp 

* American Medicine, Vol. Ill, No. 21, pp. 865, 


has degenerated, especially in cases of hypercementosis of the 
root. When degeneration of the peripheral nerves in the pulp 
takes place there may at first be pain, continuously perceptible 
to the patient or absent except under manipulation or replaced 
by analgesia. In most cases there is analgesia, owing to the 
peculiar anatomic construction of the tooth and nerve degen- 
eration. There is loss of function. The same condition exists 
in the alveolar process when diseases or intoxications occur, the 
junction of the peripheral nerves is destroyed, resistance is low- 
ered, disease of the process and peridental membrane results. 



Absorption of the alveolar process is the result of irritation, 
resultant malnutrition, and subsequent inflammation. The 
osteoblasts and osteoclasts are ever present to build up and 
tear down bone structure on the slightest provocation. Hyper- 
trophy (building up of bone tissue) is the result of intermittent 
pressure, and atrophy, or absorption of bone, is due to constant 
irritation and pressure. As has been elsewhere shown, from 
its transitory nature the alveolar process is unusually sus- 
ceptible to these influences. The causes of absorption are loss 
of teeth by extraction, undue pressure upon one or more teeth 
from improper articulation (Bonwill), wedging and irregular- 
ity correction, heat under artificial dentures, and interstitial 
gingivitis of local and constitutional origin. 

According to Kaufmann, lacunar absorption is the most 
common type. This may be true in morbid anatomy of bone 
tissue generally, but it is not true of absorption of the alveolar 
process. On an examination of hundreds of slides prepared 
from canine and human jaws (of which characteristic types are 
illustrated), by far the most common form of absorption was 
found to be halisteresis. Perforating canal absorption, which 
Kaufmann has "occasionally met with," is certainly very com- 
mon, while lacunar absorption holds third position. This order 
of absorption is accounted for by the fact that where structures 
are transitory, halisteresis, as quickest method, follows by the 
law of the survival of the fittest. For the same reason per- 
forating canal absorption should stand second. The blood ves- 
sels of von Ebner being most numerous, although considered 
smaller, would naturally be the second tissue involved. As in 
interstitial gingivitis, absorption of the alveolar process is in- 
variably due to inflammation, halisteresis apparently starts at 


the larger Haversian canals from which this form of absorption 
invariably originates. 

Interstitial gingivitis extends to the alveolar process through 
the periosteum as well as the peridental membrane (not, as den- 
tists usually believe, by way of the peridental membrane alone). 
This is demonstrated by the illustrations. The entire alveolar 
process thus becomes involved. The products of inflammation 
extend through the Haversian canals (a path obviously evident 
in pathologic illustrations), setting in action the three forms of 
absorption as elsewhere illustrated. 

Halisteresis Ossium (aoAos of salt, crrepAots deprivation) or 
decalcification, is that process of absorption wherein solution of 
the lime salts first takes place, while the cartilage or matrix 
remains for the time undisturbed. 

Solution of the lime salts begins at the periphery of the 
Haversian canal and advances toward the center of the tra- 
becular. This absorption follows, as a rule, the bone layers. 
Bone centers are, therefore, usually the last to be absorbed. 
Frequently decalcification becomes complete ; nothing remaining 
but the organic matrix or cartilage. Finally, this is also en- 
tirely destroyed. As the osteoblasts occur in the matrix or 
cartilage, it is not difficult to understand that absorption may 
extend far, yet restoration of the alveolar process may occur. 
After destruction of the matrix such a restoration is impossible. 
New fibrous tissue may be partly restored, but it is doubtful if 
the alveolar process can be. 

Both Ziegler 1 and Kaufmann 2 divide osteomalacia into senile 
and juvenile. The latter occurs most frequently during preg- 
nancy. In senile absorption, after a certain period, the entire 
skeleton is affected. The condition begins most frequently in 
the "vertebrae and thorax; later extending to the extremities." 
In pregnancy "the pelvic bones are first involved, the process 
then extends to the other bones." It is singular that the alveolar 
process should have been so much neglected by pathologists, 
since, in both states, the alveolar process becomes involved long 
before the bones of the body. 

Special Pathological Anatomy, page 151. 
' Pathologisehe Anatomie. 


This is due to three reasons: first, to trophic changes; sec- 
ond, to the alveolar process being a transitory structure; and 
third, to improper care of the gums at these periods. 

Osteomalacia occurs in the alveolar process much earlier 
than at the so-called "senile" period. It is found at twenty, or 
even earlier, and has been termed juvenile osteomalacia. At 
any period beyond that year, it occurs probably from the pre- 
maturely senile states of which precocity is a type. The lost 
tissue is regained often after confinement in the "pregnancy" 
type, but is never regained in the senile. 

The causes which produce morbid decalcification are not thor- 
oughly determined. Some believe it to be due to lactic acid in 
the system, others attribute it to an increased amount of carbonic 
acid in the blood. Eisenhart believes it to be due to a want of 
alkalinity of the blood, while von Recklinghausen charges it 
to a local irritation of the vascular mechanism of the bones. It 
would seem, from examinations already cited, that, so far as the 
alveolar process is concerned, local irritation from biochemic 
changes in the blood, as suggested by von Recklinghausen, is 
the chief cause. Premature absorption of the alveolar process 
accompanies the movement of the teeth in their correction or in 
rapid wedging. Frequently the alveolar process is never fully 
restored, thus producing a predisposing factor for future 

Premature absorption, or osteomalacia of the alveolar proc- 
ess, is easily recognized. A shrinking of the gums and alveolar 
process exposing the necks of the teeth is very conspicuous. 
Frequently the gums and mucous membrane covering the alveo- 
lar process are quite red (this is very noticeable in dogs), and a 
thinning of the alveolar process over and between the roots of 
the teeth. The process of one tooth only may become involved ; 
again the process over two, or the whole jaw, and again both 
jaws become affected. 

When osteomalacia occurs, either of pregnancy or senile 
type, although the tissues be seemingly restored to health, struc- 
tural change has taken place to such an extent that it ever 
remains a predisposing factor to interstitial gingivitis. 

In Fig. 41 may be seen the blood vessels of von Ebner. 



These blood vessels are also to be observed in Fig. 61. They 
are very common in the alveolar process and, according to Volk- 
mann, are the source of the perforating canals which bear his 

X 50. %-inch obj. No. Oc. 

Fig. 89. — Cross Section op Tooth, Alveolar Process and Peridental Membrane, 

Showing Lacunar Absorption. Man. 

C, Cementum. D, Dentine. I, Peridental Membrane. J, Alveolar Process. 

0, Lacunar Absorption. 

These canals run in all directions. After absorption has gone 
on to form medullary spaces, these canals penetrate through the 
trabecular from one space to the other (Fig. 43). The position of 
this type of absorption in the order of frequency comes from the 
fact that, in this disease, absorption is almost entirely due to 
inflammation; hence the blood vessels are the first to become 
involved. Those entering the Haversian canals, being the larger, 
are first affected, and hence halisteresis naturally precedes. 



When irritation takes place in a nerve or part of bone which 
is about to be absorbed, nmltinuclear cells arise at the border in 
the periosteum and peridental membrane. They attach them- 
selves to the surface of the bony trabecule. According to Sud- 
duth, "the absorber and the absorbed must be in touch with each 

X 300. No. 2, projection ocular. D. D. obj. Zeiss. 

Fig. 90. — Section of Peridental Membrane, Showing Lacunar Absorption in Dog. 

J, Alveolar Process. O, Lacunar Absorption. !\ [nflamed Peridental Membrane. 

other." Kolliker has named these cells " Osteoclasts," which 
term has come into general use. Very soon after these cells 
make their appearance, cavities are seen in the bone tissue. 
These cavities are called Howship's lacunae. Lacunar absorp- 
tion, as elsewhere shown, takes place as a result of irritation and 
overstimulation. Fig. 89 shows a cross section of the end of one 
of tile buccal roots of Fig. 91. As will be observed, this tooth 
was held in place by two buccal roots. As much resistance was 
required of these two roots as was formerly required of three. 


Irritation clue to excessive force in mastication was causing 
absorption. Round-cell inflammation is not present in the peri- 
dental membrane. The irritation may be continued until inflam- 
mation sets in and until the bone is entirely absorbed, as noticed 
in Fig. 90. Small round-cell inflammation is quite noticeable in 
the surrounding tissue. 

Sometimes these lacunae may be seen extending along the 
entire length of bone. As many as thirty-seven may be counted 
in some fields (Fig. 42). Lacunar absorption frequently so 
extends through the Haversian canals as to cut off pieces of the 
alveolar process. A casual glance at Fig. 89 demonstrates this. 
This figure could be multiplied many times from other slides. 
These frequently come away with the peridental membrane when 
the tooth is extracted. This is often noticed in removing loose 
teeth due to interstitial gingivitis. By passing the finger over 
the surface of the root, the rough pieces of bone may be easily 

Aside from the forms of absorption already noted, absorption 
of the alveolar process is often seen, the result of neuropathic 
lesions. Paretic dementia, diseases of the spinal cord, low forms 
of inflammation, general debility and traumatism, together with 
unhygienic conditions of the mouth, are fruitful sources of in- 
terstitial gingivitis and absorption of the alveolar process. Ab- 
sorption of the alveolar process takes place also in diathetic 
diseases in which the nervous system has been involved (syphilis, 
scurvy, lithaemia, etc.). 


There are many instances in which interstitial gingivitis 
takes place, with absorption of the alveolar process and exfolia- 
tion of the teeth, without calcic deposits. In such cases the blood 
is charged with only sufficient lime salts for the nourishment of 
the body. The waste products are carried off with the excreta. 
In absorption of the alveolar process, inflammation does not 
seem to extend to the capillaries, the result of which is, this 
waste material is carried into the circulation. In this way, 
calcic material does not collect in the fluids and upon the teeth. 
In those cases in which pus is not present (there being a lessened 
amount of carbonic acid) calcic deposits rarely take place. The 



percentage of teeth so found, however, is not so large as those 
with deposits. 

Examination, by a magnifying glass, of a recently extracted 
tooth (with the root covered with serumal deposits) shows the 
lime deposited in a manner resembling that of stalactite forma- 
tion. The deposits often stand out distinctly independent of 
each other (Fig. 91). This condition is due to deposits from the 
blood, resultant on biochemic changes in the inflamed tissues. 
Blood stasis occurs in the gum tissue, fibrous tissue of the perios- 

Fig. 91. — Palatine Root of a Molar Tooth Showing Calcic Deposits. 

teum, peridental membrane and alveolar process, through which 
last much of the blood circulates. This stasis may be consequent 
upon conditions varying from simple inflammation to disease of 
the endothelium, producing endarteritis obliterans. 

The blood has become surcharged in all constitutional dis- 
eases, but more especially in kidney lesions. Deposits occur in 
the fluids and upon the roots of the teeth. Frequently the de- 
posit is found only on one side or only at one particular spot 
on the side of the root ; again at the apex, when the pulp is de- 
stroyed. It may encircle the root. The inflammatory process 


may therefore be circumscribed as to area or the whole tissue 
may be involved. The deposit is circumscribed in the area of 
inflammation. The calcareous matter absorbed from the alveolar 
process in the immediate vicinity of the root is soon deposited 
upon the root or roots because of the impeded circulation. 3 ' ' Os- 
sification, as has been well remarked, is an active development 
in which the tissues are abundantly supplied with blood. There 
is a rapid cell proliferation, and the calcareous matter forms an 
intimate and permanent union with the tissues. Calcification, 
on the other hand, is passive, and indicates an impaired vitality. 
Calcification begins as a rule in the interstitial tissue. In regard 
to the origin of the calcareous salts, it is generally believed that 
they come more or less immediately from the blood, although 
Rokitansky supposes that they were formed by a metamorphosis 
of the tissues involved." 

Calcification is due to two varieties of causes : general and 
local. The former are dependent upon changes in the blood or 
its circulation, due, for example, to disease or senile change. In 
composition the blood may be so altered as to contain an ab- 
normal amount of calcareous matter. This effect is most com- 
monly produced by absorption of lime salts from osseous tissues 
which are the seat of extensive caries, osseous cancer, osteo- 
sarcoma or osteomalacia. The calcareous matter thus taken up 
is conveyed to other and often remote parts and there deposited, 
constituting the "metastatic calcification" of Virchow. Kiitt- 
ner, of St. Petersburg, has observed a rapid calcification of 
nearly all of the small arteries as a result of caries involving the 
dorsal and lumbar vertebrae in a nineteen-year-old boy. Virchow 
has observed a case in which, as a result of bone cancer (affect- 
ing nearly all of the larger bones, particularly the borders of the 
vertebrae and the skull), the calix and pelvis of the kidneys, the 
lungs, parenchyma, and the stomach mucous membrane were 

Circulation of the blood may be retarded and thus favor pre- 
cipitation of calcareous matter normally held in solution. To 
this is chiefly due the frequency of calcareous degeneration from 
general loss of vitality. 

Wood's Handbook of Medical Sciences, Vol. 1, page 743. 


Calcification rarely, if ever, depends upon general causes 
alone. There is, as a rule, a local influence. Very often this is 
due to pre-existing chronic inflammation. Old accumulations of 
pus and exudates are exceedingly prone to calcification. The 
deposit frequently occurs also in fibrous walls surrounding the 
accumulation. A mere loss of function predisposes to calcifica- 
tion. Such is the case in and about the tissue of the alveolar 
process. The decalcified material from the alveolar process col- 
lects in the soft tissues as well as upon the roots. In his paper 
George T. Carpenter 4 asks the question : Can a tissue be ab- 
sorbed and still remain as debris in the pocket? Such is the con- 
dition found, and this can be easily proven. Take the contents 
of a pocket and dissolve it in hydrochloric acid, add three times 
its bulk of water, to this add ammonia, which will precipitate 
the phosphate and the calcium. The same results may be ob- 
tained by rinsing a freshly extracted tooth of a pyorrhoea case 
in cold water. With a stiff brush remove the accumulation and 
place it in a test tube, add hydrochloric acid and more water if 
necessary. To this add a solution of ammonia and the lime salts 
are precipitated. 

Boots of teeth that have become entirely denuded of peri- 
dental membrane and bathed in pus accumulate large quantities 
of calcic deposits direct from the absorption of the alveolar 

Difference of opinion exists as to the nature of the process 
immediately involved in precipitation of lime salts. The sim- 
plest and seemingly most logical explanation is that the process 
is similar to that involved in the formation of stalactites. A cer- 
tain amount of calcareous matter is a normal constituent of the 
blood. Herein it is held in solution by carbonic acid, always 
present in sufficient quantity for this purpose. When the cir- 
culation is impeded the free carbonic acid (because of its great 
diffusibility) is readily absorbed by the tissues or goes to form 
new compounds, necessitating a precipitation of the calcareous 
matter. Calcareous matter may be deposited in either a fibrous 
or fluid matrix. It shows a preference for newly formed fibrous 
tissue, particularly when this is associated with old tissue under- 

4 Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhoea 


going fatty degeneration and absorption. In a fibrous matrix 
the infiltration usually begins in the intercellular substance, but 
may involve the cellular elements at a later period. In a fluid 
matrix (like pus) the granules are frequently deposited pri- 
marily within the cells. The process may advance slowly or 
rapidly. When local causes exert the chief influence it is more 
limited in area of invasion than when there is a general factor 
in its production, as in the metastatic forms. 

From research it has been shown that calcic deposits (other 
than tartar) may be due, in a limited degree, to a direct deposit 
from the blood vessels (serumal deposits of Ingersoll) while the 
greater collection upon the roots of the teeth and in the fluid 
contents of alveolar and peridental abscesses, is the deposit of 
the absorbed alveolar process. Analysis of the deposits and of 
the alveolar process as observed in Chapter VII, shows a close 
similarity between the two. 



I have shown how inflammation of the alveolar process might 
be caused by mechanical or local irritation and substances within 
the organism, without the aid of external infection, namely, irri- 
tants in the blood stream. In the last named group are to be 
included the drug and metal poisons, poisonous gases, etc., auto- 
intoxication and metabolic disturbances affecting the coats of 
the blood vessels. The alveolar process is more easily affected 
by these irritants which may set up inflammation (interstitial 
gingivitis) in a particular locality and remain there, or it may 
spread and the entire process become involved. The alveolar 
process may be destroyed by interstitial gingivitis; it is only 
necessary that there should be a low form of inflammation taking 
place in and about the arteries and capillaries to produce ab- 
sorption of bone. This is what occurs in fully ninety per cent of 

When the inflammatory exudate is made up of leucocytes, 
there is produced within the tissue small round-cell infiltration 
which becomes so thick as to obscure the tissue. When the 
leucocytes are in large numbers upon the surface of the mucous 
membrane about the cervical margin of the alveolar process 
their appearance on the inflamed surface is that of a white fluid 
called pus. Owing to the tortuous position of the blood vessels 
in the alveolar process, the thinnest part being at the gingival 
border, the inflammatory process usually begins at that point. 
The pus germs collect at the border, stasis of blood generally 
being greatest at that locality. This leads to a superficial loss 
of substance and is known as ulceration or purulent catarrh. 
When the leucocytes collect in large numbers, within the tissue, 
and are followed by liquefaction and dissolution, it is called an 
abscess. These various infections are termed pyorrhoea areo- 
laris, alveolar abscess or peridental abscess, according to the na- 
ture and location of the infection. 


Pus infection due to interstitial gingivitis, whether it pro- 
ceeds from the ulcerated surface or deep down in the interstitial 
tissues from an abscess, whether it discharges between the gum 
and root of the tooth or upon the surface of the jaw, must be 
considered pyorrhcea alveolaris, since the source of the pus is 
always in connection with the peridental membrane lining the 
socket of the alveolus. Pyorrhoea alveolaris, therefore, consti- 
tutes the second part of this study. About ten per cent of the 
patients visiting the specialist are thus infected. 

Recovery from interstitial gingivitis and return to normal 
conditions without change in structure is called restoration. 
Should the damage be extensive, and accumulations of cell and 
liquid exudate so press upon the tissues as to extinguish their 
vitality, ordinary restoration is impossible. This is also true 
when the inflammation is more decided and persistent. This 
inflammation may extend throughout the tissue. The tissues 
may be in a favorable condition for infection, yet the mouth and 
blood vessels be free from pus germs. The tissues are often in- 
vaded, however, by micro-organisms, resulting in suppuration. 
Interstitial gingivitis, with pus infection in and about the alveo- 
lar process, resembles suppuration elsewhere in the body. 

Suppuration (due to pyogenic cocci) is the usual termination 
of infective inflammation. Healthy gum tissue is intolerant of 
bacteria, and will resist the invasion of micro-organisms. When 
inflammation takes place, the diseased part is unable to resist 
them. Lowered vitality of tissue is a fruitful source of infection 
and suppuration. Since, as Miller 1 has shown, pus germs are 
found in almost every mouth, infection is a very probable out- 
come of gingivitis. 

The organisms most frequently producing pus are the staphy- 
lococcus pyogenes aureus, and albus. These have a tendency to 
accumulate in groups. When they collect at a given point in the 
tissue, suppuration results. The streptococci (occasionally pres- 
ent in the mouth) do not as a rule produce local suppuration, but 
spread through the tissue by way of the lymphatics and blood 
vessels, and eventually give rise to abscess. The delicate reticu- 
lum of the blood vessels found in the Haversian canals is a 

Micro-Organisms of the Human Mouth. 



convenient lodging place for swarms of bacteria, owing to the 
slowness of the blood current and the tortuous course of the 
blood channels. When 2 the circulation has been impeded or 
arrested by an extravasation of blood or congestion of a part, the 
conditions are favorable for intravascular infection if organisms 
happen to be circulating in the blood at the time. As we have 
seen, micro-organisms may from time to time be found in the cir- 
culation, particularly in individuals of feeble constitution. The 
anatomic nature of the part will therefore determine suppura- 
tion in certain localities. 

In whatever part or tissue the change may occur, the process 
is the same. The original structures disintegrate. Their place 
is taken by a closely packed crowd of migrated leucocytes. 
Should the cause continue to act, the process culminates in the 
formation of pus. The migrated cells cut off from proper nutri- 
tion by pressure are exposed to the injurious action of micro- 
organisms. The central cells of the group degenerate from want 
of nutrition or die from direct action of the irritation. The 
intercellular substance softens, and the liquid exudate from the 
surrounding parts mingles with the broken-down tissue to form 
an abscess. 

As I have shown, foci of infection and intense inflammation, 
to the point of degeneration and liquefaction, occur in almost 
every locality within the peridental membrane, periosteum and 
what was originally alveolar process. These abscesses are just 
as likely to point upon the surface of the gum as on the inner 
surface next to the root of the tooth. 

Abscesses in and about the alveolar process (other than those 
due to dead pulps) are very common. This is due first to the 
unstable condition of the structures, and second to the ready 
access of pus germs through the inflamed gums and peridental 
membrane. Those most susceptible to infection are patients who 
are anaemic and below par in vitality, and whose gums have 
become inflamed either from local or constitutional causes. 
Especially is this the case in those who have osteomalacia where 
the gums have receded quite a distance from the necks of the 
teeth. Pus germs collect at the necks of the teeth, infect the raw 

'American Text-Book of Surgery. 



inflamed surfaces of the epithelial layer, and entering the cir- 
culation are carried into the deeper structures. Intense inflam- 
mation results. Abscesses form, discharging- their contents upon 
the surface. Pus germs also enter the deeper structures through 
exposed pulps. 

Two cases of interest in this connection occurred recently in 
practice. An active business man, fifty-five years of age, pre- 
sented himself with an abscess over the buccal roots of the left 
superior second molar. There were no dead pulps in any of the 
teeth upon that side of the jaw. Absorption of the alveolar proc- 
ess and contraction of the gums had occurred around all the 
teeth. He had been overworked and was nervously exhausted. 
Five years ago cataracts were removed from both eyes. He is 
exceedingly sensitive to pain. Examination of blood revealed 
slight anaemia. On examination of urine, other than a specific 
gravity of 1028, it was found normal. The abscess was lanced 
and cavity cleansed. It healed within a week. Subsequently 
he returned with another abscess over the root of the right 
superior central incisor. Live pulps were in all the teeth upon 
this side as far as the second molar. Infection, therefore, must 
have occurred through the gum and peridental membrane. 

The teeth of a lady forty-six years of age were being put in 
order ; after the filling of a cavity she called attention to a space 
between the second and third superior right molars, and stated 
food lodged at that point, causing pain and bleeding. The space 
was cleansed with an excavator and the cavity syringed with 
warm water and then explored. Absorption of the gums and 
alveolar process had extended one-half the length of the buccal 
root. Applications of iodoglycerole were made to reduce the in- 
flammation. The patient was dismissed with an appointment for 
further treatment. She returned at the appointed time with an 
abscess over the palatine root as large as the thumb. The lady 
had had acute pain from the time she left the office until her 
return. The parts had become infected with pus germs through 
the peridental membrane. The pus was collected in a tin tea 
spoon, from which cultures were obtained and glass slabs 
smeared for microscopic examination. The pus was examined 


by George T. Carpenter for calcic deposits; the usual aseptic 
precautions having been taken. 

Many dentists, ignoring the laws of pathology, insist that 
intense inflammation in remote parts of the alveolar process is 
not due to toxins and irritations but is the result of gouty de- 
posits. The utter lack of foundation for this theory must be 
apparent on the slightest study of pathology. 

Ulceration is always located upon the surface of a tissue. 
When ulceration occurs from contact irritation of the gum mar- 
gin or by mechanical or chemical means, congestion and oedema 
result, thickening of the epithelial layer and increased growth of 
cells. The sub-epithelial tissue becomes inflamed. The process 
is not unlike that of the formation of an abscess, since the 
infected tissue resembles part of an abscess wall. In slowness of 
progress only does ulceration differ from acute inflammation. 

Such is the condition of the peridental membrane. When 
simple gingivitis becomes chronic, the inflammation extends to 
the surface of the peridental membrane. This is situated at the 
lower extremity of a cul-de-sac, formed by the gum on the one 
hand and the tooth on the other. This cavity is filled with for- 
eign material in which decomposition continually occurs. The 
tissues are thereby constantly irritated. Necrosis occurs at the 
surface. In the deeper tissues that have become inflamed pus 
cells also are found. These not only arise from the normal blood 
vessels in the vicinity, but also from the granulation tissue. The 
causes of peridental membrane ulceration are disturbances of 
nutrition, endarteritis obliterans (a disease of the blood vessels 
due to constitutional diseases, such as syphilis, scurvy, tubercu- 
losis, uric acid and other blood poisons) and starvation of tissue, 
feeble circulation (as in anaemia) and inflammation. If the 
ulcerated surface be examined under the microscope, a general 
thickening of the tissues will be seen. In the papillary layer de- 
posits of blood pigment occur. The surface is covered with 
granulation tissue. The tissue may, in part, resemble the type 
of healthy granulation. It is composed of round cells closely 
packed together and supplied with rich capillary network. Co- 
agulation necrosis from breaking down of granulation tissue 
may be present. 



Pus pockets start with any local irritation which sets up in- 
flammation (interstitial gingivitis) at the gingival border of the 
gums. The inflammation spreads to the blood vessels of the peri- 
dental membrane and alveolar process. Round cell infiltration 
rapidly takes place and the bone becomes destroyed, beginning 
at the gum margin or in the peridental membrane and extending 
toward the apical end of the root or to the mucous membrane 
of the mouth. The irritation which is confined to narrower areas 
may become so intense and the inflammatory exudate increase 
so rapidly that nothing remains except the fibrous tissue which 
originally held the bone cells, or the tissue becomes entirely lost. 
The leucocytes now collect in large numbers within the fibrous 
tissue and liquefaction and disintegration of tissue 1 results, form- 
ing pus pockets. 

Fjg. 92. — Thickening of the Peridental Membrane and Trabeculae (Original). 

Alveolar abscess is a term applied to an accumulation of pus 
at the apical end of the root of a tooth due to death of the dental 
pulp and other irritations. When death of the pulp occurs, de- 
composition takes place and gases form in the pulp chamber. 
The gases expand and an outlet is acquired through the end of 
the root of the tooth. These gases and other irritations set up 
inflammation in the peridental membrane, producing an alveolar 


The other irritations may be foreign substances forced 
through the end of the root or poisons in the organism passing 
through the blood stream. These irritants set up interstitial gin- 
givitis in the arteries running through the peridental membrane 
and also into the alveolar process and maxillary bone. Inter- 

Fig. 93. — Shows the Removal op the Outer Plate of Bone and Exposing the 
Eoot op the Tooth and the Alveolar Abscess (Original). 

stitial gingivitis becomes quite diffused. Bone absorption 
(halisteresis and Volkmann's canal absorption) immediately 
takes place and a considerable area of bone about the end of the 

Fig. 9-1. — Tooth With Abscess Attached Removed Prom the Bone (Original). 

root is destroyed, leaving the fibrous tissue (formerly the tra- 
becular of the bone) in a thickened condition tightly attached to 
the end of the root (Fig. 92). 



As absorption proceeds, the lime salts in the inflamed area 
are thus destroyed and the fibrous tissue or trabecular become 
organized (Fig. 93). If the tooth is extracted before liquefaction 
occurs, the fibrous mass may be removed in situ (Fig. 94). A 

Fig. 95. — Microscopic Illustration of the End of the Root of the Tooth. 
A, Omentum. B, C, Abscess attached. D, Two Points of Liquefaction. (Original). 

low microscopic section of this picture shows the end of the root 
with fibrous mass attached and degeneration and liquefaction 
of tissue just commencing at two points near the center of the 
mass (Fig. 95). A higher magnification showing round-cell 

• '<> 


z* 21 

•?▼*. V _.:»^* 

-Microscopic Al 1 

infiltration and breaking down of tissue, liquefying into pus is 
seen in Fig. 96. The pyogenic membrane forming the abscess 
walls is well shown. 



The cause of the irritation producing interstitial gingivitis 
may be so severe and active that not only is there destruction 

p 1G# 07. — Tooth Showing Formation and Destruction of Abscess With Carious 
Cavity (Original). The Irritation Which Caused the Inflammation and 
Formed the Abscess Was so Great as to Cause Destruction of the Sac. 

of bone, but also of the trabecular Under such conditions the 
root of the tooth is seen denuded of surrounding tissue (Fig. 97). 

Fig. 98. — Four Abscesses in the Peridental Membra 
Diabetic Man (Original). 


In Fig. 98 four pericemental abscesses are seen along the 
side of the root of the tooth. These are due to the lowered vital- 


ity of the individual and infection after interstitial gingivitis 
has become quite extensive. These abscesses are very common. 
The tissues about the roots of the teeth become inflamed, infec- 
tion takes place, abscesses form and discharge. The fistula heals 
without pain or inconvenience to the patient. 

In summing up this chapter on pyorrhoea alveolaris, the 
reader must not lose sight of the fact that pus infection in no 
way influences the absorption of the alveolar process and exfolia- 
tion of the teeth. It is always the primary inflammatory stage 
that causes the absorption and the pus infection is only 



Every person with pyorrhoea alveolaris has pus germs in the 
mouth which are constantly being carried into the fauces, stom- 
ach and throughout the alimentary canal. That these pus germs 
under certain conditions are destroyed in the stomach by the 
gastric juices, to my knowledge, has never been demonstrated. 
A factor unfavorable to this theory is the non-presence of the 
hydrochloric acid in the stomach except when food be present, 
whereas the saliva, laden with pus germs, is continually passing 
into the stomach and the germs must, without doubt, find their 
way into other organs, causing grave constitutional states which, 
in many instances, finally result in death. 

The degree of organic infection varies in intensity. The 
germs passing into the stomach with the food are, on account of 
the presence of the hydrochloric acid, changed in character, while 
those passing into the stomach other than during digestion, are 
more virulent and act with greater intensity upon the intestine 
and organ walls, since they produce a catarrhal condition, first 
acute which later becomes chronic. It has been shown repeat- 
edly that many stomach troubles have improved or recovery has 
been complete when the mouth has been put into an aseptic 

The influence of the stage of interstitial gingivitis known as 
pyorrhoea alveolaris on the system has been discussed by John 
Fitzgerald, 1 who points out that pyorrhoea alveolaris may act 
in three different ways in the causation of systemic disease. 
First, the pus with its multitude of putrefactive organisms and 
decayed food remnants from the pus pockets is swallowed and 
either acts locally upon the stomach wall or sets up fermentation 
of the stomach contents; second, the toxins generated in the 
mouth may be absorbed by the mucous membrane of the mouth 
or stomach and thus pass into the general circulation ; third, the 

1 Clinical Journal, March 6, 1899. 


local conditions of the mouth may favor the growth of patho- 
genic organisms and thus render the patient more liahle to cer- 
tain infectious disorders, noticeably influenza, The power of 
pyorrhoea alveolaris to produce aggravation of existing gastric 
trouble reaches its maximum in cases where there is retention 
of food residue. This happens when the muscular walls of the' 
stomach are in a state of atony and also when there is some 
pyloric obstruction which prevents the organ emptying itself. 
In both these conditions stomach dilatation is eventually pro- 
duced, with the result that the stomach is never completely emp- 
tied. The first condition is a very frequent concomitant of 
neurasthenia and allied states. It is easy to see how pyorrhoea 
can at once be predisposed to by neurasthenic states and at the 
same time increase the neurasthenia by causing gastric trouble 
through its interference with gastro-intestinal digestion under 
the conditions mentioned. 

Fitzgerald points out that the bacillus coli communis is a 
constant inhabitant of the oral cavity, and, as a rule, seemingly 
harmless. Under the influences of a culture medium, such as 
would be furnished by pyorrhoea or an inflammatory state of the 
gum, this bacteria might, as elsewhere in the mucous membrane, 
acquire sufficient virulence to produce serious disturbances of 
the system, such as colitis, dysentery and cholera nostras. 

Herschell 2 is of the opinion that many of the chronic indi- 
gestions are due to continual absorption of pus into the system 
from pyorrhoea alveolaris. In these cases he remarks there 
should be otber evidences of the absorption of toxins, such as 
pigment spots, urticaria, etc. 

Within the past few years medical thought has centered 
around the mouth and its infection as a possible cause of many 
diseases even far removed from it. The many germs of more or 
less virulence which have already been isolated in the mouth 
must of necessity affect mucous surfaces in other parts of the 
body. Medical researches have shown that diseases like per- 
nicious anaemia, arthritis deformans, all rheumatic states, bac- 
terial endocarditis, headaches, many other obscure conditions, 

Indigestion, 1895. 


etc., yield more readily to treatment when the mouth has been 
put into an aseptic condition. Every dentist has experienced the 
fact that when a poorly nourished patient has had loose teeth 
extracted, artificial ones substituted and the mouth entirely 
cleaned up, there will be increase in weight and better health. 
American and foreign journals are full of experiences of like 

Many writers who believe in the theory of the conveyance of 
pus germs throughout the body have recorded histories of pa- 
tients who are believed to have been thus infected. Some of 
these are interesting and here mentioned to show what serious 
constitutional conditions take place from an unhygienic condi- 
tion of the mouth and teeth. 

There are many affections of the tonsils, neck glands, etc., 
directly traceable to the septic condition of the mouth and teeth. 
Especially is this true of school children. Stewart 3 reports 231 
cases of tonsil enlargement in which 135 had a caried condition 
principally of the lower molars on the enlarged tonsil side; 67 
had caries and an unhygienic mouth ; 16 had no septic condition 
of the mouth and 15 had caries and a septic state on the opposite 
side. He also mentions cases of laryngitis which yielded to 
treatment after putting the mouth in an aseptic state. 

It has long been known that nearly all glandular conditions 
are dependent upon bacterial infection of more or less virulency. 
Many cases of gland infection have been shown to be directly 
due to a septic condition of the mouth. A case coming under the 
author's notice was that of a twenty-three-year-old man whose 
original mouth condition of pyorrhoea alveolaris was augmented 
by a local spirrilla infection. After being under treatment for 
some weeks with no recovery results, he was referred to me. I 
found the gums, peridental membrane and alveolar process in a 
severe inflammatory state with pus oozing from the tooth 
sockets. The neck glands were enlarged on both sides and tender 
to touch. After the mouth was put in an aseptic state, the glands 
became their normal size and the tenderness disappeared. 

"Stewart, C. J. Oral Sepsis in its Connection With Throat Diseases. The Lancet, 
June 25, 1902, p. 1882. 

'Hunter, W. The Lancet, 1900, 1904. 


Hunter * reports a case of gastritis which he claims is directly 
due to infection from the mouth. A sixty-two-year-old woman 
was suffering with subacute gastritis. There was severe pain 
and intermittent sickness, so much so that morphia was often 
resorted to. The illness had been of eight months' duration 
coupled with loss of weight and great weakness. Examination 
for cancer of the stomach, abdomen, rectum or uterus revealed 
nothing. There was continually a bitter taste in the mouth, 
nausea and loss of appetite. Examination of the vomit found it 
filled with streptococci, staphylococci and a few bacilli. There 
were three roots of teeth remaining in the mouth from whose 
sockets there was a constant flow of pus. With the extraction 
of the roots the stomach condition was benefited. 

It has been a much discussed question among physicians as 
to whether gastric ulcers are not directly due to a septic condi- 
tion of the mouth, but convincing proof has not been evidenced 
since gastric ulcers are known to occur in persons with healthy 
mouths. In the chronic ulcer type, however, an unclean mouth 
with pus coming from the tooth sockets is the rule. 

Dr. Frank Billings, in a paper on ' ' Chronic Focal Infections 
and Their Etiologic Eelation to Arthritis and Nephritis" 5 
speaking of the site of local infection, mentions "the faucial 
tonsils, abscesses of the gums and alveolar sockets, pyorrhoea 
alveolaris and septic types of gingivitis may also cause systemic 
diseases of various types. The systemic results of focal infec- 
tion are: 1. Chronic arthritis is one of the most common re- 
sults. 2. Nephritis, both acute and chronic. 3. Cardiovascular 
degenerations. 4. Chronic neuritis and myalgia (myositis)." 
He says further, ' ' The studies and experiments embodied in this 
paper are limited to the arthritides and to subacute and paren- 
chymatous nephritis. Of these, chronic deforming arthritis, com- 
monly known as arthritis deformans, and chronic osteo-arthritis 
of hypertrophic or atrophic type, comprise the majority of the 
studies. Next to the arthritides the largest number of cases com- 
prises subacute parenchymatous nephritis and chronic paren- 
chymatous nephritis. The work has been done on private and 
clinic patients in the Presbyterian Hospital. The bacteriologic 

" The Illinois Medical Journal, March, 1912. 


and histologic studies and the animal experiments have been car- 
ried on by Dr. D. J. Davis and by Dr. Homer K. Nicoll." 

Ten cases of arthritis and six cases of subacute and chronic 
parenchymatous nephritis are described. Among this number 
case Number III is worthy of special mention here. 

Case 3. — Mrs. E. W., aged 50 years. I-para. Osteoarthritis 
chronica, mixed type. Admitted to the Presbyterian Hospital 
Oct. 16, 1909. For two years there had been swelling, tender- 
ness, pain upon motion and deformity of many of the joints of 
extremities. Began in feet and hands and extended to larger 
joints and finally involved cervical spine. The condition was 
progressive. There was malnutrition, loss of weight from 160 
to 120 pounds. For years the patient had been subject to attacks 
of acute tonsilitis. She had also suffered for years from pyor- 
rhoea alveolaris. 

Examination : Poorly nourished, very nervous and irritable. 
Mouth badly infected, many stumps of carious teeth, some of 
them loose in the sockets, gums retracted and infected, tonsils 
large, rough, adherent to pillars of fauces and crypts infected. 
Breath offensive. Heart, lungs, abdominal organs and pelvic 
organs normal. There was swelling with some deformity of 
both ankles, right metatarsojDhalangeal, both knees, right middle 
and left fingers, the wrists, and elbows. Some contraction of 
hamstring muscles prevented complete extension of legs. Both 
bicep tendons of the arms contracted which prevented extension 
of the forearm. Twenty-four hours ' collection of urine was nor- 
mal in amount and specific gravity and contained a few hyalin 
casts. Blood : Hemoglobin, 90 per cent ; reds, 4,600,000 ; whites, 
13,400. On Oct. 18, 1909, both f aucial tonsils were enucleated by 
Dr. George E. Shambaugh and one week later the roots of cari- 
ous teeth were removed by Dr. Frederick Moorhead. From the 
cut surface of the tonsillar tissues a pure culture of streptococcus 
was obtained. A rabbit inoculated with a culture suffered from 
acute multiple arthritis and died in a few days. The strepto- 
coccus was regained from the infected joints and from the 
heart's blood. The patient was permitted to return to her home 
too soon and did not fully carry out directions as to rest treat- 
ment. Some time elapsed before the alveolar processes were 


absorbed and the mouth remained sore. On April 3, 1910, she 
returned to the hospital, where rest treatment was instituted 
with resulting marked improvement. The patient gained in 
weight from 129 to 140 pounds. After the return home fre- 
quent communications by letter with the patient and her physi- 
cian have shown that the progress of the disease has entirely 
stopped. Some of the deformities were so great that one could 
not expect entire anatomical restoration. The last communica- 
tion is dated December, 1911, in which the patient says that the 
strength of her upper extremities and spine is entirely normal. 
There is some fatigue in the lower extremities after attempting 
to walk for any great distance, but there is a continued improve- 
ment even in this respect. 

All the cases cited in this article are of unusual interest be- 
cause they are based upon researches and actually demonstrate 
the source of infection and the results of such infection upon 

Osier says of the twenty cases of pernicious anaemia which 
he had under observation in 1909, pyorrhoea alveolaris was pres- 
ent in more than half. Certain types of nephritis are also be- 
lieved to be due to oral infection. 

Zilz 7 reports four cases of cysts at the roots of teeth in which 
bacteriologic investigations revealed the presence of Much's 
granula, which he defines as the non-acid-fast form of the 
tuberculosis germ. The findings are profusely illustrated and 
the questions discussed are "why it is so difficult to detect acid- 
fast, Gram-staining bacilli in the gangrenous pulpa," and "why 
primary tuberculosis starting in carious teeth is not of more 
common occurrence." He regards Much's granula as merely 
ordinary acid-fast tubercle bacilli which have lost their acid-fast 
properties ; hence the organic fluids are able to disintegrate them 
and the vital centers, the granula, escape into surrounding me- 
dium. When conditions become more favorable to the bacilli, 
they may become impregnated again with acid-fast substance 
and the acid-fast form thus develop again, which in turn may 
break up anew into granula. His plates show the process dis- 

1 Practice of Medicine, p. 440. 
Beitriige zur Klinik der Tuberkulose, Wiirzburg, Vol. XXII, No. 2, pp. 97-264. 


tinctly, the granula causing no tuberculous changes in the dental 
cyst. The bacilli probably found their way through the blood 
into the cyst and while there remained latent but regained their 
virulence when conveyed farther to lymph-nodes or lungs. In- 
oculation of animals with the granula always gave positive 

W. Hunter 8 has repeatedly called the attention of the pro- 
fession to the close relationship existing between the mouth 
infection and the various forms of anaemia, particularly the per- 
nicious type. He contends that the pus taken into the stomach 
produces an unhealthy state of that organ and also the intes- 
tines, thereby favoring the destruction of the red blood cells. 

In all forms of arthritis there is an association in the condi- 
tion of the mouth. The disease stamps itself indelibly upon the 
alveolar process. There is gum recession and absorption of the 
alveolar process of more or less intensity and pus infection. 

A case referred to the author for treatment of the mouth is 
of more than passing interest. The patient, a twenty-seven- 
year-old woman, unmarried, had been a sufferer from arthritis 
deformans for many years. For ten years previous to her com- 
ing to me she had been unable to leave her home except when 
carried. The entire osseous system was involved, but more 
especially the extremities. The hands had become so malformed 
and stiff that she was unable to pick up or hold anything. The 
mouth was in frightful shape. There were loose teeth with pyor- 
rhoea alveolaris, absorption of the gums and alveolar process, a 
number of large cavities, tartar and calcic deposits. After the 
loose teeth had been extracted, the tartar and calcic deposits 
removed, the cavities filled, an artificial denture inserted and 
the pyorrhoea alveolaris treated, the constitutional condition 
commenced to improve. At the end of three months she could 
walk with the aid of crutches, in six months with only the use of 
a cane, and at the end of a year had no use for either. The stiff- 
ness in the hands disappeared to such a degree that she could 
use them. She has now recovered to such an extent that she is 
able to assist in the housework. 

The Lancet, 100(1, ]904. 


Dr. Kenneth Groadby, 9 of London, England, reports four in- 
teresting cases of arthritis which are worthy of consideration at 
this time. They are as follows : 

Case 1.— A girl, aged twenty-two, was attacked somewhat 
suddenly by swelling of the hands and feet and fever lasting 
two or three weeks. With the subsidence of the fever the joints 
did not return to their normal size but remained painful and 
stiff ; walking was almost impossible. The affection was bilateral 
and the swelling was evidently peri-articular, and to a limited 
extent affected the synovia of the joints, but no fluid was dis- 
covered. Treatment at Bath and a long course of salicylates 
produced little improvement. There was no family history of 
rheumatism or of gonorrheal infection and no septic focus was 
thought to exist. On examination of the mouth, the right upper 
central incisor was missing, the teeth and gums were apparently 
quite normal. A closer examination revealed a small sinus lead- 
ing up to the root of the missing central incisor and a film made 
from the sinus showed a large number of pus cells loaded with 
organisms. Cultures were made and an organism was isolated 
in practically pure culture ; the blood tested against this organ- 
ism gave a very low opsonic as well as a low phagocytic index. 
A vaccine was prepared and injections given, commencing with 
ten million dead bacteria. After four injections the sinus was 
opened under a general anesthetic and was found to lead into a 
cavity in the bone about the size of a small hazelnut. This was 
cleared out with a sharp spoon and the lateral incisor also was 
removed, the cavity extending under its root and invading the 
periosteum of the tooth. The improvement of the joints which 
had commenced with the inoculations received a slight tem- 
porary setback as the immediate result of the operation, but 
improvement soon recommenced with continued vaccine therapy 
and the patient has steadily improved and is almost well. 

The second case is that of a man of thirty-eight years. He 
was suffering from acute pain and swelling in both knees and 
both feet, ulnar deflection of both hands and acute pain and 
swelling on the dorsal aspects, fluid and deformity of the left 
elbow joint and of the left shoulder joint, ansemia and neuras- 

The Practitioner (London), January, 1012. 


thenia, partly owing to the constant pain and partly toxic. I 
may note in passing that secondary septic neurasthenia is com- 
mon in cases of oral infection, probably due to the long-continued 
infection with small doses of bacterial toxins. The patient had 
been under all sorts of treatment, residence at Continental and 
English Spas, had been to the Canary Islands, had taken vast 
quantities of iodid of potassium, had had massage, electric baths, 
ionisation and "Christian Science" and all with no avail. 

His mouth was a veritable gold mine ; he had two bridges, two 
in the upper, two in the lower jaw, and four gold crowns in addi- 
tion to the bridges; pus was welling up from his gums in all 
directions. The builder of the bridges told him he could do noth- 
ing for him as he had rheumatism in his gums. He was treated 
by the removal of all the crowns and bridges and by vaccines 
made from his two organisms. He made a slow but steady recov- 
ery and is now enabled to resume his ordinary avocation which 
he had been obliged to give up for three years previous. Unfor- 
tunately the right knee-joint is partially disabled owing to 

The third case, a man aged forty, in March, 1908, had a sud- 
den attack of pain behind the left ear, progressive stiffness and 
muscular rheumatism and stiffness of the right shoulder and 
right hip joints. Ten days later, rigor, temperature 102° F. and 
evening temperature of 100° F. for two or three weeks which 
gradually subsided. In the following spring another acute attack 
with fever, pains in the head and neck, swelling of sterno-mastoid 
sheath and stiff neck, lasting five weeks. An X-ray photograph 
of the chest was taken and it was thought the case was one of 
early tuberculosis ; the patient was sent to a sanatorium where 
he derived no benefit. He was in constant pain, unable to move 
his head, and had constant attacks of fever at night, the tem- 
perature running up to 100° F. and falling to subnormal in the 
morning. He became wasted, losing more than a stone in weight, 
was greatly depressed mentally and had to give up his work. 
On examination in October, 1909, considerable thickening was 
found in the left shoulder joint and right knee joint. The left 
sterno-mastoid was thickened in the region of the rectus, capitis 
posticus and complexus, and thickened tender areas along the 


spine process of the cervical and dorsal vertebrae. Hyperes- 
thesia over all cranial nerves. The patient could walk only with 

The molar teeth had been lost on both sides in both jaws. 
The patient resented any suggestion that his mouth was at fault, 
as he had recently seen his dentist who pronounced his gums and 
teeth quite sound, and the gums appeared normal in color. 
Careful examination with a fine platinum probe brought to light 
several deficiencies between the remaining teeth and passing 
down to bare bone, and microscopically pus was demonstrated. 
A vaccine was therefore prepared and inoculations were per- 
formed. The patient made an uninterrupted recovery, the inoc- 
ulations were discontinued and a slight relapse took place. The 
vaccine was therefore continued for a further six months. The 
patient made a complete recovery. 

In the fourth case, a woman aged forty-two, there was a 
severe general infection of the mouth. All the teeth were loose 
and copious discharges of pus came from all sockets. There had 
been chronic progressive arthritis for the last four years asso- 
ciated with occasional acute exacerbations, constant pain in both 
knee joints which were swollen and thickened, especially the ex- 
ternal and lower portions of the capsule; creaking was well 
marked in the knees and shoulders, with ulnar deflection of the 
right hand. All teeth were removed and considerable improve- 
ment took place. Six months after removal of teeth pain re- 
curred in the right knee and in the shoulders but passed off. A 
year later, eighteen months after removal of teeth, the pain and 
stiffness of the knees again recurred together with fusiform 
swellings and local vasomotor disturbances of the fingers. On 
examination the gums were found quite healed; there was no 
inflammation, but small patches of thickening were seen along 
the outer surfaces of the alveolar process. A puncture was made 
into these and a pure culture of the streptobacillus make was 
found. Vaccine therapy was instituted and the rheumatoid symp- 
toms rapidly disappeared and two years later no recurrence 
had taken place. 

Every specialist has noted the marked improvement in his 
patients, some of whom were suffering with obscure ailments, 


after having loose teeth removed, pyorrhoea alveolaris treated 
and cured, gums and mouth placed in an hygienic condition, 
artificial teeth inserted to fill vacant spaces, and many expe- 
riences could be recorded. 

Gilmer 10 reports three interesting cases. He says, "Some 
years ago, a man, a little beyond middle life, consulted me rela- 
tive to a trivial dental lesion. On making a careful examina- 
tion of the entire oral cavity, I found several small sinuses dis- 
charging pus above the bicuspid teeth on one side of the upper 
jaw. On exploring these openings with a sharp steel probe a 
large cavity was discovered in the bone, the result of alveolar 
abscess, the presence of which was unsuspected by the patient. 
On inquiring into his physical condition I learned that for the 
past year he had had a cough, his digestion was impaired, and 
much of the time his temperature was slightly above normal. 
He had frequently consulted his family physician who examined 
his heart, lungs, sputum, urine and blood. These gave no clue 
to the cause of ill health. His appearance indicated a toxemia. 
I removed several teeth, curetted the abscess in the jaw and 
followed it by suitable after-treatment. His fever at once sub- 
sided, his digestion was soon much improved, his cough was 
lessened and finally disappeared altogether. Although seem- 
ingly his physician had made a careful examination he had 
overlooked one important factor, the mouth. 

"Mrs. C, aged thirty years, noticed the appearance and dis- 
appearance at frequent intervals of an erythemic patch about 
the size of a silver quarter on the skin over the left canine fossa. 
On examining the mouth for a possible cause for this reddened 
condition of the skin I found the left lateral incisor pulpless. 
There was no sinus and the tooth had given no trouble. The 
only evidence of disease found in the mouth was a slight hyper- 
emia of the gum over the lateral incisor root indicated. The 
radiograph showed a pus cavity in the bone at the end of the 
root about the size of a large pea. Disinfection of the root did 
not effect a cure. I made an opening through the labial wall of 
the alveolar process, excised the end of the root and curetted 

10 The Illinois Medical Journal, March, 1912. 


the cavity. The erythemic patch on the cheek disappeared and 
did not return. 

"Mr. S., aged about twenty-five years, was directed to my 
clinic for the treatment of a chronic abscess in the upper jaw 
in the vicinity of the incisors and cuspid which had proven in- 
tractable to ordinary treatment. His physical condition was 
much impaired, he was emaciated, his skin was sallow, his 
cheeks hollow, his conjunctivae pale, eyes dull, and his lips lacked 
the color of health. His temperature was slightly above normal. 
I could elicit no history of any other illness, recent or other- 
wise. His appearance gave the picture of a toxemia. In this 
case, likewise, the sharp steel probe revealed a large cavity in 
the bone, extending from the central incisor to the first molar. 
On Oct. 20, 1911, I extracted the cuspid tooth and curetted the 
bone cavity. On Oct. 27th, he returned to the clinic much im- 
proved. Nov. 10th, his color was normal, his eyes clear, and he 
seemed well." 

Dr. T. B. Hartzell, of Minneapolis, reports the following 
four cases: 

"Case 1. A typical case of pyorrhoea alveolaris. Patient, 
male, aged 50 years. Molar and bicuspids in both lower and 
upper arches freely movable in sockets, having lost the bone 
to about one-half of the original depth of sockets, pus discharg- 
ing freely from the sockets about the teeth, temperature nor- 
mal, specific gravity of urine 1018, no albumen, no sugar. Pa- 
tient reports a tender area in the stomach wall. Diagnosis, 
ulcer of the stomach accompanied by chronic dyspepsia. Patient 
has had treatment for ulcer of the stomach for two years with 
but temporary benefit. The treatment in this case was first ex- 
traction of two of the loose teeth followed by accurate planing 
of the root surfaces of all the teeth which had lost alveolar 
process. Absolute cessation of pus flow. Gums resume normal 
tint and after two months no tenderness in the region of the 
ulcer, digestion about normal. 

"Case 2. Male, aged 48. Chronic pain and tenderness in the 
masseter muscles of the left side. Tenderness of the sublingual 
glands and torticollis. Tenderness of left shoulder joint. Ex- 


animation of the mouth revealed dead pulp in left lower 8 with 
free pus discharge from deep pyorrhoea pockets. Left lower 6 
and 7 vital pyorrhoea pockets one-third the depth of the root. 
General pyorrhoea of all the molars and bicuspids on both sides 
of the mouth. Chronic acid indigestion with constant eructa- 
tion of gas after the ingestion of food. Treatment, extraction 
of loose left lower 8. Planing of the root surface of all the 
teeth affected by pyorrhoea. Pockets were pencilled with tinc- 
ture of iodin. After two weeks, rheumatic pains in shoulder 
and tenderness of sublingual glands disappeared. Digestion 
improved. End of fourth week all inflammatory symptoms con- 
tiguous to the teeth absent. Teeth no longer tender on occlu- 
sion. Patient has resumed vigorous mastication of food. End 
of two months all symptoms of dyspepsia absent. This case is 
typical of a group of five cases in which joint involvements have 
been present from one to three years which have all disappeared 
upon the stamping out of oral infections. 

"Case 3. Mrs. J., aged about 50, with mild inflammation of 
the gum margins. Abscess in the region of left upper 2 pen- 
etrating the palatal tissues an inch and a quarter. Patient 
enjoys moderately good health though a constant sufferer from 
constipation, rheumatism of the arms, wrists and fingers, and 
of the feet, ankles and knees. Pains sufficiently sharp on rising 
to cause marked discomfort. Draining of the abscess and treat- 
ment of the interstitial gingivitis results after two months in 
complete freedom from rheumatic pain and also freedom from 

"Case 4. Miss A., aged 26, suffered chronic dyspepsia and 
neurasthenia. Has been treated for three years in various 
sanatoria and has also spent two winters in Southern Califor- 
nia. Patient presented the winter of 1906. Mentally, much 
depressed. Physically, very weak. Weight, 86 pounds. No 
albumen, no sugar. All the teeth exceedingly loose. Deep 
pockets discharging pus freely. Teeth all extracted except four 
in the upper and four in the lower jaw. These eight teeth were 
treated for pyorrhoea and although they were so placed that they 
were of no value for mastication the patient showed a marked 
improvement. At the end of one week had gained one pound in 


weight although obliged to subsist largely upon liquids. Arti- 
ficial dentures were placed, and the patient increased in weight 
steadily at the rate of a pound a week until her normal weight 
of 106 pounds had been regained, after which time she returned 
to her home. ' ' 

Dr. David J. Davis, 11 Pathologist of St. Luke's Hospital, re- 
ports the following: " Pyemia, septicemia, meningitis, neuritis, 
endocarditis, etc., as acute infections originating from alveolar 
abscesses and infected food about the teeth, are well known oc- 
currences. Chronic generalized or systemic infections are rarer 
and less commonly recognized. As an illustration I may men- 
tion briefly one rather striking case which came under my 

"A young man had been suffering for several weeks with 
symptoms of severe multiple neuritis associated with some 
anaemia, marked emaciation and slight fever. The joints were 
not involved and physical examination revealed no heart lesion. 
For a long time the patient had been troubled with severe pyor- 
rhoea and at the time of examination the gums of the lower jaw 
were red and swollen, bled easily and on pressure abundant 
pus exuded from between teeth and gums. Smear and culture 
examination of this pus revealed, in nearly pure growth, many 
Gram-positive diplococci resembling pneumococci. The colonies 
produced a green zone on blood-agar and the organism acidi- 
fied and coagulated milk and fermented inulin. A blood-culture 
made by taking several cubic centimeters of blood from the vein 
at the elbow yielded in each of three inoculated culture-tubes a 
pure growth of the same diplococcus. In animals this organism 
was not highly pathogenic. One broth-culture intraperitoneally 
would kill guinea-pigs in twenty-four to forty-eight hours. Two 
rabbits were inoculated repeatedly with large amounts of cul- 
ture without manifesting serious or fatal effects. Apparently 
these diplococci are identical with the cocci often found in endo- 
carditis and called endocarditic cocci and they are also probably 
identical with the diplococcus almost constantly found in the 
mouth and usually called Streptococcus viridans (Schottmiiller . 
I may say, too, that they appear to be the same as the diplococci 

"Archives of Internal Medicine, April, 1912. Vol. IX, pp. 505-514. 


which I have found at times in the tonsillar crypts, especially in 
cases of endocarditis, and which I will discuss later in the paper. 
In this particular case the tonsils were carefully examined and 
appeared to be normal and no suspicious foci of infection other 
than the teeth could be held accountable for the condition. 
Unfortunately, the patient did not remain long under observa- 
tion and the termination is not known. ' ' 

Dr. Edward E. Rosenow of the Pathological Laboratory, 
Rush Medical College, says, in a letter to the author, "Clinical 
observation convinces me that the low grade infections about the 
teeth, etc., which are looked upon so often as harmless, are far 
from being so. The evidence is practically conclusive that endo- 
carditis may have its origin in some such infection. In the Sep- 
tember number of the Journal of Infectious Diseases there will 
appear an article on endocarditis in which these points will be 
taken up. The mechanism of how the organisms which are so 
common in these infections about the teeth can produce endo- 
carditis is shown experimentally in the rabbit." 

At the meeting of the American Medical Association held at 
Atlantic City in June, 1912, Dr. E. Libman of New York exhib- 
ited in the pathological exhibit a series of twenty-two hearts 
showing bacterial endocarditis due to mouth infection. 

Medical literature records many ailments and cures of dis- 
ease associated with pus infection in the mouth. While every 
practitioner would logically reason from his every-day experi- 
ences that there is a relationship existing between cause and 
effect, yet more absolute data in the way of research is neces- 
sary to show more clearly that such relationship exists. The 
work of Billings, Rosenow, Davis and others should be con- 
firmed by many more experiments upon animals to verify these 

The author is one of those who believes that infections of 
the mouth are taken into the stomach with every swallow; and 
that infection of the glands of the neck as well as absorption of 
pus directly into the blood and carried to all parts of the body, 
occurs in a large percentage of our patients, because he has 
cured many thus infected and improved the health of others by 
putting the mouth in a healthy condition. 



The treatment of interstitial gingivitis as a whole is very 
unsatisfactory both to the operator and the patient. The clin- 
ical history of each structure is essentially that of any other 
disease of the mucous membrane, periosteum and bone tissue. 
From a microscopic viewpoint, however, as illustrated by the 
author's researches, the pathologic aspect is quite complicated, 
since the relation of tooth, peridental membrane, alveolar proc- 
ess and gum tissue has no counterpart in any other part of the 

The etiology of most of the disease to the dentist is obscure 
in nearly every person under treatment, as there are consti- 
tutional factors involved in connection with the local irritation. 
The dental specialist not having a medical education and a gen- 
eral knowledge of disease intoxications, the faulty metabolism 
and lowered resistance are not understood. 

There is a general law in medicine laid down many years 
ago that to treat a disease successfully the cause must always 
be removed. In those patients in whom the cause is of a consti- 
tutional nature, there may or may not be local deposits. The 
mere cleansing of the tooth roots and local treatment will not 
always cure such conditions. On the other hand, much harm 
may be caused (as we have already shown) by local irritation, 
traumatic lesions, and changes in function which cause the tissue 
to be readily acted upon by irritants in the blood stream. A 
large percentage of interstitial gingivitis is influenced or en- 
tirely due to constitutional causes. Interstitial gingivitis 
under such circumstances can never be permanently reduced 
until the cause has been ascertained and remedied. A very thor- 
ough history of the patient, especially age and condition of the 
urine, should be obtained. Such data will assist the specialist 
greatly in a clear understanding of his method of procedure. 

We have shown that the tooth, so far as this disease is con- 


cerned, is a foreign body and the alveolar process is an endo- 
transitory structure. When disease, therefore, whether due to 
local or constitutional causes, once affects these structures, even 
if they be restored to comparative health, they are more easily 
involved than other structures of the body. When inflammation 
has once taken place in these tissues, whether the disease be due 
to local or constitutional causes, the operator may apparently 
restore these structures to health. If, however, the cause is not 
removed, whether it be local or constitutional, the disease soon 
returns as it is of a progressive nature. This necessitates fre- 
quent visits of the patient for further treatment. The endo- 
transitory nature of the alveolar process, after inflammation has 
once affected the part, naturally causes the disease to become 
chronic. The obscure constitutional causes and the chronic ten- 
dency of the disease soon causes the tooth to become loose and 
finally exfoliated. 

When the disease is taken in hand and continually treated 
before the bone becomes involved, a fair success may be ob- 
tained. I have demonstrated that bone absorption around the 
teeth as one grows older is a natural process which cannot be 
arrested to any extent. Toxins and irritations assist greatly, 
dependent always on the resistance of tissue and strength of 
the irritant. Neglect on the part of the patient to massage the 
gums properly twice a day and use a proper gum wash, the 
irritants in the blood and in the mouth, cause the tissue to soon 
return to their pathologic state when the bone becomes dis- 
eased, owing to its endo-transitory nature. Chronic inflamma- 
tion once set up, "eternal vigilance" on the part of the oper- 
ator and patient is the only method that will prevent the disease 
from progressing with a final destruction of the alveolar process 
and exfoliation of the teeth. 

The disorder responds quickly to treatment at its outset. 
Later, its complications and the extent of structure involved, 
render treatment very inefficacious, and always insure loss of 
the tooth. As the general surgeon's duty is to save life, if need 
be, at the expense of limb or organ, but to save these last if pos- 
sible, so the dental surgeon's duty is to remove loose teeth, if 
need be, for the benefit of the gene i *al health, but to save them, 


when possible, for the same reason. The patient, therefore, 
should be told frankly at the outset of interstitial gingivitis, 
that it is a condition requiring time for its treatment, and should 
not be given that prognosis too frequently made of quick cure. 
To such a prognosis many a case of constitutional disorder is 
due. The dentist is a practitioner of a surgical specialty, not a 
mere tooth-puller. The surgical side of dentistry has received 
too much attention, however; the medical or prophylactic too 
little. Patients are beginning to pay more attention to the pro- 
phylaxis of diseases of the teeth and jaws, and need but little 
encouragement and instruction to see the absolute necessity of 
early prophylaxis and treatment of interstitial gingivitis. The 
trend in general medicine is to prophylaxis, and this has un- 
doubtedly so impressed patients as to open the way for dental 
prophylactic suggestions. Viewing the question from the narrow- 
est standpoint of remuneration, the dentist could not fail to profit 
by instructions to his patients on prophylaxis. He certainly 
fails in his duty as the member of a learned profession by not 
doing this. Furthermore, with the known necessity for pro- 
phylaxis, it is an open question whether the failure to inform 
the patient of the dangers of the incipient disease could not be 
successfully pleaded as a basis for a malpractice suit. 

From the etiology of this disease, the treatment would ap- 
pear simple and easy. 

Early diagnosis is not difficult, since the simple inflammation 
of the gums is easily recognized by the patient. Bleeding when 
the toothbrush or toothpick is used can never be mistaken. 
The dentist with his accomplished eye can readily detect the 
slightest change in color or puffiness around the necks of the 
teeth or of the festoons between the teeth. Redness, puffiness 
and bleeding are pathognomonic of this disease in its incipiency. 

Few dentists have, however, given this stage of the disease 
any thought, albeit they have filled the teeth of their patients 
from year to year. I have in mind three patients with loose 
teeth and inflammation extending throughout the peridental 
membrane and alveolar process, who had been under an old 
practitioner now retired from practice. The patients had never 
had the gums treated or even their teeth cleaned. This is not 



an uncommon occurrence. The excuse usually made by the den- 
tist is that he cannot get paid for his time. Gingivitis is a dis- 
ease which the dentist is as much bound to treat and cure as any 
disease of the mouth and teeth. It is a part of his specialty 
which should not be ignored. It is claimed that the dental pro- 
fession is overcrowded. Were this disease treated until the 
gums were placed in a healthy condition, there would be prac- 
tice enough for as many more dentists as there are today. The 
busy dentist of today could attend only to one-half the patients 
whom he now serves. 

The treatment, then, should be prophylactic in its nature, 
preventive rather than corrective. The disease and treatment 
is not unlike an inverted pyramid : the farther from the apex or 
beginning, the more difficult and hopeless the task becomes. 
Since the teeth have nothing directly to do with this disease, 
they should be ignored. In the early stages, the gums should 
receive proper attention. These, like other parts and organs of 
the body, must be exercised and kept clean to be healthy. The 
gums should be properly massaged, just as the liver, kidneys 
or skin are when they are not doing proper work. This can be 
accomplished by properly made brushes. The ordinary tooth- 
brush is not adapted to the work under discussion. It will 
brush the teeth but not reach the gums. What is needed is a 
massage brush that will miss the teeth to a certain extent, but 
will reach the gums and contract them tight around the teeth, 

Author's Otm Massage "Brush. 

thus preventing the accumulation of foreign substances. The 
patient should be instructed with this single idea in view, "that 
the gum margin is to be exercised and stimulated and not the 
teeth, which must be ignored." A brush, properly made for 
gum massage (Fig. 99), will do sufficient work upon the teeth 
with the aid of the floss silk and toothpick. It should have 


printed upon the handle, in large letters, ''gum massage 
brush." The handle should be bent a little more than the "pro- 
phylactic," so that the end containing the bristles can be 
brought in contact with the gum, posterior to the central in- 
cisors, upper and lower, and around the third molar teeth. 
There should be a tuft of bristles at the point with a space for 
the teeth. The tuft should be longer than those on the body of 
the brush. This tuft will reach the gums at all points inside of 
the mouth and around the molars. The bristles on the body 
must have spaces between them, so that when the upward and 
downward movement is given, the bristles will go between the 
teeth and reach the gum festoons. The bristles must be medium 
and hard. The quality of bristles must depend, however, upon 
the condition of the gums. If they be soft and spongy, the 
medium may be used. If the processes are heavy and thick, the 
gums swollen and engorged with blood, hard bristles must be 
used. Soft bristles (although sometimes recommended) should 
never be used. 

The antique theory that vigorous stimulation is injurious is 
too much accepted. Barrett, 1 for example, says, "massage of 
the gums with the ball of the finger and by the frequent use of a 
rather soft brush should be resorted to." Bcedecker 2 remarks 
that too frequent application of the toothbrush is sufficient to 
produce papillary hyperplasia. Tomes 3 says, "in my own expe- 
rience I have found that frequent and vigorous rubbing of the 
gums with the finger, shampooing them in fact, has often been 
productive of great advantage, the patient of course being cau- 
tioned not to rub the actual edge; but even on this point there 
is difference of opinion, for in a recent paper on the subject, 
rest and the avoidance of all friction is advocated. ' ' Dr. Meyer 
L. Ehein, 4 in introducing the "Prophylactic Toothbrush" to the 
profession, says, in his article on "Oral Hygiene," each brush 
comes inclosed in an envelope, upon which are printed directions 
for the intelligent use thereof, and the following caution: 
"Never pass the brush across the teeth, as this movement de- 

1 Dental Cosmos, 1883, page 532. 

3 Anatomy and Pathology of the Teeth, page 365. 
8 Dental Surgery, page, 704. 

4 New England Journal of Dentistry, October, 1884. 


stroys the delicate membrane which attaches the gum to the 
teeth, causing recession of the gum, and ultimate loosening and 
loss of the teeth." Citations of this could be multiplied, show- 
ing the general impression is that the gums should not be stim- 
ulated to any great extent ; that the finger, a soft cloth, or a very 
soft toothbrush alone should be employed. The use of the finger 
is a superstition which is handed down from generation to gen- 
eration without the slightest critical analysis. If the advocate 
of this use would try the experiment, he would see how impos- 
sible it would be to bring it in contact with all the tissues of the 
mouth that are involved in this disease; were it possible, the 
fingers, cloth and soft toothbrush would not accomplish the 
desired result. 

No brush should be used whose bristles are softer than the 
medium; very often these, used once or twice and dipped into 
water or mouth washes, become so soft as to be wholly unfit for 
use. It is always a good plan to have two brushes to be used on 
alternate days. In this way one can dry while the other is being 
used. The general opinion has been that friction upon the gums 
was detrimental on account of the resultant tendency to absorp- 
tion of the gums. While this may exceptionally be true, it is 
not true of a majority. Should milk, arsenic, iron, strychnine or 
quinine be entirely abolished as remedies because occasionally a 
person presents untoward effects? If the alveolar process be 
very thin over the roots of the teeth, especially the cuspids, the 
patient must be instructed to use the brush so as not to over- 
stimulate these particular parts. In such cases the inner alveo- 
lar process and gum tissues may be stimulated with impunity 
and with the hardest brush. Again, if the chronic interstitial 
gingivitis be of long standing, or even if chronic gingivitis has 
been present for some time, stimulation of the brush will cause 
the gums and mucous membrane to recede until hard, sound, 
healthy bone structure has been secured. Then absorption for 
the time being will practically cease. In most cases absorption 
and contraction of the gum tissue will take place to a more or 
less marked degree. If absorption of the alveolar process has 
taken place and the gums are puffy, red and swollen, a disease 
exists, to be cured, regardless of consequences. The alveolar 


process and gums will never return to their original position, 
but it is a decided advantage to have a healthy mouth, even if 
the alveolar process and gums have slightly receded. 

I have used medium and stiff brushes in my practice for the 
last thirty years and have failed to see any ill results. For the 
past sixteen years I have made constant experiments, with the 
view of securing the proper shape and stiffness of the bristles 
and have obtained uniform results in gum treatment. 

Proper employment of the "gum massage brush" requires 
skill. Every dentist should train his patient in the method of 
using the brush. The gingival borders should not only be stim- 
ulated, but the bristles should be passed in between the gum 
margin and the tooth so as to remove the debris and exfoliated 
epithelial scales which have accumulated therein. These are 
often the cause of the irritation. Unless this is done the gum 
or epithelial tissue cannot perform its functions or be restored 
to health. Stimulating astringents and germicidal mouth 
washes should be employed whenever the gums are massaged. 
One of the best gum washes is that suggested by Dr. W. H. 
Whitslar, 5 of Cleveland, Ohio, the principal drug of which is 
sulphocarbolate. This drug may be used in different strengths 
and in many forms. I use the following: 
Gum Wash. 

Zinc sulphocarbolate gr. 60 

Alcohol oz. 1 

Distilled water oz. 2 

True oil of wintergreen gtts. 8 

The massage should be done three times a day. The patient 
should be under the care of the dentist at least twice or thrice 
a week, so that he may direct the treatment. If the teeth are 
irregular, care and patience are required to reach the festoons 
between the teeth. After the gums are in perfect health, the 
patient should visit his dentist at least four times a year, or 
even oftener if necessary, for inspection. If on inspection the 
gums be found diseased at any point, the dentist can direct the 
attention of the patient to the particular locality and the disease 
be eradicated. By this method and this alone can the gums be 

Dental Summary, 1907, No. 8. 



kept in a healthy condition. Each patient must be given specific 
directions as to the treatment of his or her case. 

When the patient seeks our services, we should decide by a 
thorough examination whether the disease is due to local or 
constitutional causes or both. The age of the patient, condition 
and character of deposits, if any, condition of mouth, jaws and 
dental arches, condition of urine, occupation and everything 
pertaining to the patient should be considered. While this ex- 
amination is being conducted, which requires a few days, the 
local treatment may be undertaken. This consists of an appli- 
cation to the mouth, gums, mucous membrane and teeth of a 
germ destroyer every other day until the parts are in an aseptic 
condition as far as possible. 

I cannot here too strongly condemn the method of starting 
the treatment of this disease by scraping the roots of teeth 
which may or may not have calcic deposits, wounding the soft 
tissues and infecting them without first rendering them as 
aseptic as possible. Asepsis is always the first precept of the sur- 
geon before any kind of an operation. Why should the dentist 
be exempt from similar methods? It is fortunate for the den- 
tist that stasis of blood prevents infection to a great extent or 
serious results might occur. 

This, however, does not justify the vicious treatment em- 
ployed, since the method of procedure is wholly unscientific and 
not in harmony with good practice. 


The operator is not justified in placing his fingers in the 
filthy mouths of his patients. This is also true of the students 
in the clinics of our dental schools. It is in the clinic where the 
student should be taught the object lesson of cleanly mouths 
before operations. No patient in the clinic or in private prac- 
tice should be operated upon before a thoroughly aseptic mouth 
has been obtained. The method is so simple and so easily per- 
formed that only a few minutes is required before operation 
may be commenced. This treatment should consist of the free 
use of iodin applied to the gums and teeth, carrying it well up 
into the pockets. This will destroy every germ with which it 
comes in contact. After many years of experimentation, sur- 


geons have come to realize that iodin is the quickest acting and 
best germicide we now possess. The author, when he began his 
researches in 1878, commenced the use of iodin and has used 
it to the exclusion of all other drugs in the treatment of this 
disease. The results obtained are all that can be desired. 

The official tincture of iodin contains seven per cent of iodin 
dissolved in alcohol to which is added five per cent of potassium 
iodid. This preparation, if used often, will cause the membrane 
to become tender and sore ; it will also, in some patients, destroy 
the mucous surface. To overcome this difficulty, many years 
ago, I formulated the following which I have called 
iodoglycerole : 

Zinc iodid 15 parts or grams 

Water 10 parts or grams 

Iodin 25 parts or grams 

Glycerin 50 parts or grams 

As compared with the ordinary tincture of iodin, its astrin- 
gent and antiseptic properties are greatly increased, the glycerin 
causes rapid absorption and the irritating effects are reduced 
to a minimum. The penetrating effect is remarkable. The 
glycerin thickens the preparation and prevents it from mixing 
with the saliva and running over the mouth as the ordinary 
tincture will do. Long, round, wood applicators can be obtained 
at the drug and instrument houses and on one end cotton is 
wound; this is saturated with the preparation and the gum 
margins above and below painted. The jaws are closed, the 
lips and cheeks distended and the application made as before; 
the teeth are also covered; the lips and cheeks are held away 
from the jaws until the iodin has dried. 

These applications should be made every other day and con- 
tinued until the patient is dismissed. In a fairly clean mouth, 
the process of removing the local causes may be commenced at 
the second appointment or possibly at the first sitting after the 
iodoglycerole has become dry. In the more filthy mouths, the 
time to commence operations will depend upon the judgment of 
the operator and the condition of the mouth under treatment. 

In those patients who are having operations upon the teeth, 


although their gums are in fairly good condition, they are treated 
after each sitting to destroy lactic-acid bacilli and their ferment 
and all other foreign and undesirable material in the mouth, 
thus preventing tooth decay. By this method of procedure, I 
have reduced decay of the teeth from thirty to forty per cent 
in my patients in the past ten years. While this treatment is 
being conducted by the operator, the patient should use the gum 
wash twice a day as directed. After the patient has been dis- 
missed the gum wash should be used continually once a day. 

Having destroyed all the germs in the mouth including pus 
germs (except perhaps in so-called pockets out of reach with the 
iodoglycerole) and contracted the gums, more or less, about the 
necks of the teeth and on to the bone, exploration of the mouth 
for local irritants and irregularities may now be undertaken. 

Erupting Teeth, whether the first or second set, should be 
examined by the operator and the inflamed gums receive the 
iodoglycerole treatment. This procedure should be continued 
in the public schools among the poor children as well as at the 
homes of the well-to-do. If the iodoglycerole gum bath was 
introduced into the public schools, contagions and infections 
would be reduced to a minimum. 


I have stated that modern dentistry has produced disease of 
tiic gums, pericemental membrane, and alveolar process more 
than any one cause. The education of the student in the dental 
schools in the mechanics of dentistry has been conducted to the 
exclusion of the pathology of the mouth. The mechanics have 
been carried far beyond normal physical tolerance. The dis- 
covery that pus formation in alveolar, pericemental and blind 
abscesses and the accumulation of pus about the alveolar proc- 
ess and roots of the teeth cause many of the diseases of the 
human body is a just evidence of the necessity of a medical edu- 
cation of the dentist. Xot until the methods of teaching have 
been reconstructed, can we expect any improvement from the 
pathologic standpoint in the management of the month and teeth. 
The local causes which bring about interstitial gingivitis have 
been discussed in Chapter XYI1 and every teacher and practi- 
tioner is familiar with them, hence it is hardly necessarv to 


discuss the question here. It is to be hoped that the profession 
will soon consider the pathology of our specialty and so far as 
possible correct and prevent local irritations, inflammations and 

In passing this subject, however, there are a few suggestions 
which may be offered here. There is no excuse for the whole- 
sale movement of teeth without extraction. The specialist 
should make a study of the jaws and teeth of each patient to 
ascertain how much may be accomplished with as little move- 
ment of the teeth as possible. This is to be frequently accom- 
plished by the sacrifice of one or more teeth. The health of the 
patient, as well as the causing of as little inflammation in the 
alveolar process as possible, should be the foremost thought in 
the mind of the operator. The frequent use of iodoglycerole is 
indicated during the operation of correcting irregular teeth to 
keep down the inflammation. After the retaining bands have 
been adjusted the iodoglycerole should often be used. 

We have shown that the condition of the alveolar process, 
especially after it has attained its growth and its endo-transi- 
tory nature, is a very unfavorable structure for the successful 
operation for the implantation or transplantation of teeth, par- 
ticularly so when the peridental membrane is not present. 

Gold Ckowns and Bands should only extend to the gum mar- 
gin and never above it except in extreme cases. 

Artificial Dentures should be so constructed as to produce 
the least amount of irritation possible. The larger the surface 
the better the adaptation. Iodoglycerole treatment to the sur- 
face of the mucous membrane under the plate to destroy germs 
and reduce inflammation should be frequently applied. 

Individual Teeth whose function is not restored from want 
of proper articulation — too great or not sufficient pressure — 
must be corrected. Such teeth are liable to become diseased, like 
any other organ or structure of the body when not properly 
exercised takes on pathologic changes according to the tissue 

Tartar upon the teeth acts as a local irritant and should 
always be removed. In some mouths it accumulates rapidly and 
must be removed as often as once a month ; in other mouths no 



tartar is present. The teeth in such patients should be cleaned 
as often as twice a year. These suggestions, however, are only 
given out approximately, since the operator must decide by the 
conditions as they exist how often visits should be made to 
obtain the best results. Having destroyed the germs in the 
mouth and about the teeth by the free use of iodoglycerole, the 
tartar may be removed without fear of infecting the tissues and 
with a large degree of comfort to the operator on account of a 
clean mouth. Laceration of the gums in performing this oper- 
ation is desirable. It removes the excess of stagnant blood from 
the tissues and greatly assists in restoring normal circulation. 
Three decades ago, I advocated the following set of scalers : 

They consist of handles, shanks bent at different angles, and 
three cornered blades, so that they can be used in three direc- 
tions without removing the fingers from the tooth (Fig. 100). 

2 3 4 5 6 

Fig. 100. — The Author's Set of Scalers. 
These are all delicately made and tempered very hard. Sharp 
edges are thus retained. They will reach every point where 
tartar can collect. After the deposits have been fairly well re- 
moved, the gums may be syringed with hot water to remove 
the debris. The gums should then be saturated with iodoglycer- 
ole and the patient dismissed. Applications should be made 
every two or three days. The gums will contract and healthy 
circulation follow. The gum massage with the gum wash will 



now be used twice a day. After a few treatments and the con- 
stant use of the massage brush, the gums will contract and other 
deposits which were not perceptible at the first sitting will now 
be presented to view. This method of treatment should be con- 
tinued until the gums and alveolar process are restored to 
health. The patient should return to the dentist as often as 
necessary (every month or two) to have the gums examined 
and for further instructions. 

As has been already shown, chronic interstitial gingivitis 
may extend only to the peridental membrane, to the periosteum, 
or it may extend throughout the alveolar process with the ab- 
sorption of the bone the entire length of the root of the tooth. 
Pus infection and calcic deposit may or may not take place. In 
the early stages of this progressive inflammation, the first is 
probable. If pus and deposits are present they can be treated 
with signal success according to the symptoms and as herein- 
after explained. As already suggested, the gum massage brush 
must be vigorously used to relieve the engorged tissues of blood. 
Since absorption of the alveolar process depends upon irritation 
and inflammation, this must be removed as quickly as possible. 

In the treatment of deep-seated interstitial inflammation, 
iodin or iodin and aconite has always been regarded by physi- 
cians and surgeons as the best remedy. The gums should be 
thoroughly saturated twice or thrice weekly, as already sug- 
gested. If the alveolar process be so absorbed that the tooth has 
become loose, the case is hopeless. In such unstable tissues, 
especially when inflammation extends through the process and 
lacunar, perforating canal absorption and halisteresis is going 
on, reversal of the order so as to set the osteoblasts to tissue- 
building is hardly to be expected. The tendency is to destroy 
and not restore the alveolar process. In such cases the tooth 
must be fastened to the other teeth perfectly tight to prevent 
motion in any direction. The movement of the tooth in masti- 
cation intensifies the irritation, which in time only increases the 
absorption. Liberal use of iodin and the gum massage brush is 
all that can be done to reduce the inflammation and absorption 
as much as possible. The exfoliation is only a matter of time. 
If the tooth or teeth cannot be retained perfectly tight, no mat- 


ter how healthy the surrounding tissues may he restored, the 
irritation produced by the loose teeth will soon set up inflam- 
mation in the surrounding tissues. The sooner the loose teeth 
are removed the better. In no ease can the bone tissue be re- 
stored, if the matrix or cartilage be destroyed, since in this the 
osteoblasts are located. If the matrix or cartilage be destroyed, 
a fibrous union (such as occurs in the case of implanted teeth 
and the imbedding of foreign bodies in the tissues of the body) 
only is possible. 

If inflammation has extended into the periosteum, peri- 
dental membrane and alveolar process, calcic deposits are fre^ 
quently found upon the roots of the teeth. When this has taken 
place, the calculus must lie removed. This should be done with 
the utmost care, in order that adjacent tissues may not be in- 
jured, or inflamed parts infected with pus germs. Since dead 
bone is not present, the operator should confine his instrumenta- 
tion entirely to the root or roots of the teeth, with as little injury 
as possible to the adjacent tissues. The alveolar process must 

Pjg. 101. — Spoon Shaped Excavators for Scaling the Roots of Teeth. 

under no consideration be touched. Riggs believed that the edge 
of the alveolar process was always in a state of disintegration, 
and that it should be so scraped as to get a fresh surface, on the 
principle of caries of bone. Many dentists are operating in this 
manner at the present time. I have elsewhere shown simple 
absorption and not caries is present. Such treatment is wholly 
unnecessary and contraindicated. The object of the removal of 
the deposits is to allow the fibrous tissue of the peridental mem- 
brane (after health is restored) to tighten about the root, which 
eannol be accomplished when foreign substances are present. 


Pushing instruments must never be used, but only such instru- 
ments as have smooth and round backs, tempered very hard so 
as to retain sharp edges. These instruments should be small, 
with small points to reach depressions, and to be as universal 
as possible. Such an instrument is to be found in the spoon ex- 
cavator (Fig. 101). The shank can be bent to suit the operator. 
This is to be carried gently along the length of the root and 
passed over the deposit with a firm hand, resting the finger upon 
some other teeth. The drawing motion is invariably to be from 
the membrane, and toward the crown. Attention was first called 
to the mutilation and infection of tissues two decades ago, at 
which time most, if not all, instruments for the removal of deep- 
seated calcic deposits were used with the pushing movement. 6 
The deposits are scaled off painlessly. The round blade being 
larger than the shank, and cutting upon three edges, half of the 
root in both directions can be circled without removing the in- 
strument. A similar instrument bent at the shank in the oppo- 
site direction may be used on the other side. After all of the 
roots of the teeth have been scaled, the spaces are to be syringed 
out with warm or hot water. The gums are to be thoroughly 
saturated inside and out with iodin. The gum massage brush is 
to be used thrice daily as before. The patient should return 
twice or thrice a week for further instructions. The contracting 
gums will assist greatly in revealing the deposit. If deposits 
still remain on the roots (the appearance of the gums will indi- 
cate its presence) further use of the scalers is indicated. The 
delicate instruments and the accustomed sense of touch will 
reveal the hidden calculus. 

With the precautions already noted, local anaesthesia is 
unnecessary. The smooth, round surface of the back of the 
instrument, if carefully inserted, will not produce pain. 

If the gum be painful to the touch, or if the patient be 
nervous and sensitive, application of iodin may be used, to- 
gether with massage, for a few days before scaling is resorted 
to. The sensitiveness will soon disappear, when the instrument 
may be inserted without difficulty. 

Jour. Am. Med. Assoc, Jan. 16, 1897. 
International Dental Journal, April, 18£ 


In an article upon "Pyorrhoea Alveolaris," 1 T showed the 
difficulty of removing the deposits upon the roots of the teeth 
with instruments and made the following statement: '.'From 
our past experience in the treatment of the disease, the deposits 
must he removed; and right here I would suggest that in the 
future treatment of this disease a dissolving fluid that is not 
injurious to the surrounding tissue should take the place of 
instruments, especially when the disease is extensive." 

I am pleased to state at this time that Dr. Joseph Head, in a 
paper, "A Tartar Solvent, Especially Useful in Pyorrhoea 
Work," 8 in which he demonstrated his experiments upon the 
action of acid ammonium fluorid as a solvent for calcic deposits, 
claimed to produce good results without action upon the tooth 
structure or soft tissue. This preparation, known as "Tarta- 
sol," can he obtained at any of the dental depots. This or sim- 
ilar drugs and the method of application must eventually 
become the proper treatment for the satisfactory removal of 
deposits upon the roots of the teeth. In this way and this alone 
can we expect to obtain a clean, smooth root surface. A few 
years hence, the profession will regard a dentist whose patients 
have pus oozing from the gums as a prehistoric relic and the 
patient as an individual whose filth provokes the contempt of 
his fellows. In this day of antisepsis, the dentist is as account- 
able for pus infection of his patients as the physician or surgeon. 

There is no more excuse for the dentist's patient being in- 
fected than the surgeon's. If ordinary antiseptic precautions are 
taken, pus infection will not often occur. Prevent inflammation 
of the gum margin and pus infection cannot follow, no matter 
how many germs are in the mouth. This is an absolute law of 
general pathology. It has been proven by the experiments made 
by Miller, G. T. Carpenter and myself on dogs, rabbits, guinea 
pigs and man. 

The illustrations of the progress of interstitial gingivitis 
teach that only the mildest treatment is indicated. Harsh treat- 
ment on the inflamed bone or fibrous tissue, either with instru- 
ments or drugs, must not be employed. Heroic treatment, such 
as the indiscriminate application of sulphuric and lactic acid and 

Transactions National Dental Association, 1899, 


similar drugs in nearly or quite full strength, is not justified by 
the surgical principles of today. No surgeon would think of mak- 
ing such an application to inflamed bone in other parts of the 
body unless he wished necrosis with a desired sequestrum. 
Much less would the intelligent operator use such treatment in a 
transitory structure which predisposed to destruction. In a 
number of instances exfoliation of the anterior plate of the alve- 
olar process has resulted from this treatment, to say nothing ot 
the intense pain produced. J. M. Whitney 9 has had four cases 
in his practice in which serious results followed. The first indi- 
cation is to remove the cause. Instrumentation should be re- 
sorted to only to remove tartar and calcic deposits. This must 
be done in such a manner as not to infect the deeper inflamed 
tissue or carry the products of inflammation into healthy tissue. 
The treatment of infected tissue within and about the alveoli is 
not unlike treatment of abscesses and ulceration elsewhere. 
Such drugs as are used in abscesses and ulcers in other tissues 
are indicated here in the same strength. If strong drugs be 
used they should not be permitted to remain in the tissue, lest 
necrosis of the alveolar process occur. They must be diluted or 
removed altogether after they have accomplished their purpose, 
Very serious results have occurred from careless use of drugs. 
When abscesses have formed they should be opened and hydro- 
gen peroxid — or, which has answered my purpose equally well, 
hot water — is all that is necessary. More difficult is treatment 
of ulceration of the tissue near the root of the tooth. Ordinary 
cases will heal after hot water or hydrogen peroxid have been 
applied. In some cases the pus germs have followed the inflam- 
mation along the course of the vessels quite a distance into the 
interstitial tissue. In such cases they are difficult to reach. A 
small syringe may be employed, or the drug may be carried to 
the part on the end of a long, thin orange-wood stick. In all 
cases the drug must be directly applied to the part in order to 
have beneficial results. Applications of iodin should be used, 
as already suggested. Iodin carried to the ulcerated surface 
often suffices to destroy the pus secretion. Ordinarily one or 
two applications is sufficient. Occasionally calcic deposits are 

International Dental Journal, April, 1890. 


located in front of the infected surface and the drug does not 
reach the part. In such cases the deposit must be removed. If 
the pus does not cease at the first, second or even third appli- 
cation, this is not because the drug - is not sufficiently strong, but 
because it does not reach the infected part. Continued applica- 
tions of iodin externally and internally, carried well up between 
the roots of the tooth and the alveolar process will, in time, pro- 
duce the desired result. When pus ceases to flow, antiseptic 
treatment must stop. The iodin and massage treatment must 
then be pushed until the interstitial inflammation has been re- 
duced and the gums contracted tightly about the necks of the 

After the tissues have been placed in a healthy condition, 
they will require the constant attention of the operator, since, 
like other tissues of the body when once diseased, favorable con- 
ditions will cause a recurrence. The patient must return to the 
operator frequently so that he can advise as to the use of 

When constitutional disorders are the cause of interstitial 
gingivitis, local treatment will not cure the disease. It is pos- 
sible to deplete the parts of blood and reduce the inflammation 
to a minimum. The cause not having been removed, the inflam- 
mation soon returns. 

When the disease is due to constitutional causes, tartar de- 
posits rarely occur; scraping the roots, therefore, is useless. 
Pus germs may or may not be present. The local iodoglycerole 
treatment, however, is indicated, but the constitutional causes 
of the disease must be considered by a competent physician. 
The history of the patient must be looked into, a complete uri- 
nary examination made and the heart pressure taken. The 
heart, liver, kidney, bowels, lungs and skin must be placed in a 
healthy condition; without this attention local results are impos- 
sible. Change in climate and food frequently benefit the patient, 
Loose teeth must be fastened tightly to other teeth; this, how- 
ever, is only temporary, since (as I have already mentioned) the 
function is lost. Better results can be obtained by their removal. 



In the treatment of a disease by vaccine, it is positively 
necessary that the exact nature and identity of the germ or 
germs producing the disease be known. It is also necessary that 
the various types of infections as well as the pathologic condi- 
tion in which the bacteria are present as secondary infections 
be known. 

This knowledge will prevent the specialist from using a vac- 
cine which will not immune the germs which produce the disease. 

The technique of this treatment is of so much importance 
that I cannot express my views better than to quote from an 
article, "The Principles of Bacterin Therapy," by Dr. J. Favil 
Biehn, 10 "The corresponding bacterins are indicated in all bac- 
terial infectious diseases; but since the bacterins have a spe- 
cific action only, it is absolutely essential to know the particular 
organism or organisms causing the disease under treatment and 
to give the corresponding bacterins. Thus, for instance, bacil- 
lus-coli bacterins are of value only in diseases caused by the 
bacillus coli ; they are practically valueless in diseases caused by 
other organisms. Hence, there are no bacterins for such ail- 
ments as boils, furuncles, and the like, for these conditions are 
not always produced by the same organism or group of organ- 
isms. In one case streptococci, in another case staphylococci 
(either albi or aurei) may be the etiological cause. The first 
form will be benefited only by the bacterins containing strepto- 
cocci, while the second responds only to one containing staphylo- 
coccus albus, etc. However, a mixed bacterin may be employed, 
and will prove beneficial, provided it contains the specific organ- 
isms responsible for this particular diseased condition. 

"Therefore, unless the exact etiologic cause is determined 
and the corresponding bacterins are administered, failure will 
surely result. It is quite necessary, in case several pathogenic 
bacteria are acting together in producing a disease, that the cor- 
responding bacterins for all of them be utilized ; and further, if 
the infection should change as a result of the invasion of other 
organisms unless a bacterin for these organisms is also used, a 
complete cure may not be obtained." 

10 American Journal of Clinical Medicine, February, page 157. 


A careful study of the researches in this work will show that 
interstitial gingivitis is due to local and constitutional irritants 
and toxins and not to infections. 

The operator must not lose sight of the fact that it is the 
inflammatory condition which causes the absorption of the alve- 
olar process, and the exfoliation of the teeth and not the pus 
stage. The pus formation is the result and not the cause of the 

While it is possible that a vaccine may be made, of the pus 
germs which cause the secondary state of the disease (pyorrhoea 
alveolaris), which may possibly render these germs innocuous 
and stop the flow of pus, such treatment can, according to our 
present knowledge, hardly be expected to reduce the primitive 
stage (interstitial gingivitis) so much to be deplored. It is barely 
possible that in the future specific germs may be discovered 
which may cause the inflammatory stage. When this has been 
accomplished, a vaccine may lie produced which will be a posi- 
tive method of treatment. Until then the vaccine method of 
treatment should be used with discretion. 


The following books and monographs 
of the author have been drawn on largely 
for material in compiling the present 


i. The Irregularities of the Teeth, First 
Edition, 1888. 

2. The Irregularities of the Teeth, Sec- 

ond Edition, 1890. 

3. Chart of Typical Forms of Irregu- 

larities of the Teeth, 1891. 

4. A Study of the Degeneracy of the 

Jaws of the Human Race, 1892. 

5. The Etiology of Osseous Deformities 

of the Head, Face, Jaws, and 
Teeth, Third Edition, 1894. 

6. Degeneracy: Its Signs, Causes and 

Results (London), 1898. 

7. Interstitial Gingivitis or So-called 

Pyorrhoea Alveolaris, 1899. 

8. Irregularities of the Teeth, Fourth 

Edition, 1901. 

9. Quiz Compend of Irregularities of 

the Teeth, 1901. 

10. Irregularities of the Teeth, Fifth Edi- 

tion, 1903. 

11. Developmental Pathology; A Study 

in Degenerative Evolution, 1912. 

1. Education, Dental Colleges — The 

Dental Cosmos, 1876. 

2. Mercury, Chemical and Physiolog- 

ical Action of Fillings on the Sys- 
tem — The Denial Cosmos, 1879. 

3. Preparation of Nerve Canals for 

Treatment and Fillings — The 
Dental Cosmos, 1880. 

4. Gold Crowns — The Dental Cosmos, 


5. Screws for Artificial Crowns — The 

Dental Cosmos, 1881. 

6. Treatment and Filling of Approx- 

imal Cavities — The Dental Cos- 
mos, 1881. 

7. The Regulation of Teeth by Direct 

Pressure — The Dental Cosmos, 

8. Dental Regulating Apparatus — The 

Dental Cosmos, 1885. 

9. Spreading the Dental Arch — The 

Dental Cosmos, 1886. 

10. Regulating Individual Teeth — The 

Dental Cosmos, 1886. 

11. Pyorrhoea Alveolaris, 1st Paper — 

The Dental Cosmos, 1886. 

12. The Etiology of Irregularities of the 

Teeth— The Dental Cosmos, 1888. 

13. Arrest of Development of the Maxil- 

lary Bones, due to Race Crossing, 
Climate, Soil and Food— The 
Dental Cosmos, 1888. 

14. Development of the Inferior Maxil- 

la by Exercise and Asymmetry 
of the Lateral Halves of the 
Maxillary Bones — The Dental 
Cosmos, 1888. 

15. Asymmetry of the Maxillary Bones 

— The Dental Cosmos, 1888. 

16. The Alveolar Process— The Dental 

Cosmos, 1888. 

17. The Origin and Development of 

the V and Saddle Arches and 
Kindred Irregularities of the 
Teeth— The Dental Cosmos, 1889. 

18. The Above Concluded— The Dental 

Cosmos, 1889. 

19. Classification of Typical Irregular- 

ities of the Maxillae and Teeth — 
The Dental Cosmos, 1889. 

20. Statistics of Constitutional and De- 

velopmental Irregularities of the 
Jaws and Teeth of Normal, Idiot- 
ic, Deaf and Dumb, Blind and 
Insane Persons — The Dental Cos- 
mos, 1889. 

21. Fallacies of Some of the Old Theo- 

ries of Irregularities of the Teeth 
with Some Remarks of Diagnosis 
and Treatment — The Dental Cos- 
mos, 1890. 

22. The Teeth and Jaws of a Party of 

Cave and Cliff Dwellers— The 
Dental Cosmos, 1890. 

23. The Differentiation of Anterior Pro- 

trusions of the Upper Maxilla 
and Teeth, International Medical 
Congress, Berlin — The Dental 
Cosmos, 1890. 

24. Mouth-Breathing not the Cause of 

Contracted Jaws and High Vaults 
— The Dental Cosmos, 1891. 

25. Management of Dental Societies — 

The Dental Cosmos, 1891. 

26. Studies of Criminals — The Alienist 

and Neurologist, 1891. 

27. Scientific Investigation of the Cra- 

nium and Jaws — The Dental Cos- 
mos, 1891. 

28. Evidence of Somatic Origin of Ine- 

briety — Journal of Inebriety, 1891. 



29. A Study of the Degeneracy of the 

Jaws of the Human Race — The 
Dental Cosmos, 1892. 

30. Empyema of the Antrum — Journal 

of the American Medical Asso- 
ciation, 1893. 

31. The Vault in its Relation to the 

Jaw and Nose — The Dental Prac- 
titioner and Advertiser, 1894. 

32. Stigmata of Degeneracy in the Aris- 

tocracy and Regicides — Journal of 
the American Medical Associa- 
tion, 1894. 
353. The Degenerate Ear — Journal of 
the American Medical Associa- 
tion, 1895. 

34. Pyorrhoea Alveolaris, 2nd Paper — 

International Dental Journal, 
1896; The Dental Cosmos, 1896. 

35. Dental and Facial Evidence of Con- 

stitutional Defect — The Interna- 
tional Dental Journal, 1896. 

36. H. H. Holmes — Journal of the 

American Medical Association, 

37. Pyorrhoea Alveolaris, 3rd Paper — 

Journal of the American Medical 
Association, 1896. 

38. Degeneracy of the Teeth and Jaws 

— Journal of the American Medi- 
cal Association, 1896. 

39. Oral Hygiene — International Medi- 

cal Congress, Moscoiv, 1897. 

40. Autointoxication in its Medical and 

Surgical Relations to the Jaws 
and Teeth — Journal of the Amer- 
ican Medical Association, 1897. 

41. Pyorrhoea Alveolaris in Mercurial 

and Lead Poisoning and Scurvy, 
4th Paper — Journal of the Ameri- 
can Medical Association, 1898. 

42. Degeneracy in its Relation to De- 

formities of the Jaws and Irregu- 
larities of the Teeth — The Chica- 
go Dental Review, 1898. 

43. A Study of the Stigmata of Degen- 

eracy among the American Crimi- 
nal Youth — Journal of the Ameri- 
can Medical Association, 1898. 

44. Irregularities of the Dental Arch — 


45. A Study of the Deformities of the 

Jaws among the Degenerate 
Classes of Europe — The Interna- 
tional Dental Journal, 1898. 

46. Inheritance of Circumcision Effects 

— Medicine, 1898. 

47. What Became of the Dauphin Louis 

XVII? A Study in Dental Juris- 
prudence — Medicine, 1899. 

48. Interstitial Gingivitis due to Auto- 

intoxication — The International 
Dental Journal, 1900. 

49. Traitement de la Pyorrhie Alveo- 

dentaire — XIII International Med- 
ical Congress Proceedings, Paris, 

50. The Intervention of Therapeusis in 

Anomalies of Position and Direc- 
tion of the Teeth — XIII Interna- 
tional Medical Congress Proceed- 
ings, Paris, 1900. 

51. Limitations in Dental Education — 

Journal of the American Medical 
Association, 1900. 

52. Interstitial Gingivitis from Indiges- 

tion Autointoxication — Journal of 
the American Medical Associa- 
tion, 1900. 

53. Interstitial Gingivitis as a Promi- 

nent Obvious Early Sympton of 
Autointoxication and Drug Poi- 
soning — Chicago Medical Society 
Proceedings, 1901. 

54. Peridental Abscess — Proceedings 

Ne<w York State Dental Society, 
1901. The Chicago Dental Re- 
view, 1 901. 

55. Oral Manifestations and Allied 

States — Journal of the American 
Medical Association, 1901. 

56. Degeneracy and Political Assassina- 

tion — Medicine, 1901. 

57. The Higher Plane of Dentistry — 

Revue de Stomatologic, Paris 

58. Juvenile Female Delinquents — The 

Alienist and Neurologist, 1901- 

59. The Stigmata of Degeneracy — The 

Medical Examiner and Practi- 
tioner, 1902. 

60. Deformities of the Bones of the Nose 

and Face — The Laryngoscope, 

61. Evolution of the Pulp — Journal of 

the American Medical Associa- 
tion, 1902. 

62. Why Dentists do not Read — The In- 

ternational Dental Journal, 1903. 

63. How Far do Stomatologic Indica- 

tions Warrant Constitutional 
Treatment? — The International 
Dental Journal, 1903. 

64. Syphilitic Interstitial Gingivitis — 

The International Dental Journal 

65. Gum Massage — The International 

Dental Journal, 1903. 

66. The Vasomotor System of the Pulp 

— Journal of the American Medi- 
cal Association, 1903. 

67. Recognition of the D. D. S. Degree 

bv the American Medical Asso- 
ciation — Dental Journals, 1903. 

68. What the Physician or Surgeon 

should know of Dentistry — Illi- 
nois Medical Bulletin, 1903. 



Pathogeny of Osteomalacia or Senile 
Atrophy — Journal of the Ameri- 
can Medical Association, 1904. 

Constitutional Causes of Tooth De- 
cay — The Dental Digest, 1903. 

Interstitial Gingivitis or So-called 
Pyorrhoea Alveolaris — The Dent- 
al Summary, 1903. 

Buccal Expressions of Constitutional 
States — Medicine, 1903. The 

Dental Digest, 1903. 

Endarteritis Obliterans and Arterio- 
sclerosis of the Alveolar Process 
— The Dental Digest, 1903. 

Pathology of Root Absorption and 
Alveolar Abscess — The Dental 
Digest, 1904. 

The Relations of the Nose and Geni- 
talia — Medicine, 1904. 

Pulp Degeneration — -Journal of the 
American Medical Association, 

Criminal Responsibility and Degen- 
eracy — British Medical Associa- 
tion, Section on Psychological 
Medicine, 1904. 

Anatomic Changes in the Head, 
Face, Jaws and Teeth in the 
Evolution of Man — Fourth Inter- 
national Dental Congress, St. 
Louis, Mo., 1904. 

Constitutional Causes of Tooth De- 
cay, Erosion, Abrasion and Dis- 
coloration — Fourth International 
Dental Congress, St. Louis, Mo., 

Etiology of Cleft Palate— Fourth 
International Dental Congress, St. 
Louis, Mo., 1904. 

Scorbutus or Interstitial Gingivitis 
— Medical Neics, 1904. 

Negro Ethnology and Sociology — 
Illinois Medical Bulletin, 1905. 

Gonorrhoeal Ulcero-Membraneous 
Stomatitis — The International 
Dental Journal, 1905. 

Evolution of the Central Nervous 
System — The Dental Digest, 1905. 

Study of the Pithecanthropus Erectus 
or Ape-Man — The International 
Dental Journal, 1905. 

Advance and Retrogressive Evolu- 
tion— The Dental Digest, 1905. 

Underlying Factors of Development- 
al Pathology or Suppressive Evo- 
lution — The Denial Digest, 1905. 

Laws Governing Eugenesis: A 
Thirty-five Years Study of Devel- 
opmental Pathology — The Dental 
Era, 1905. 

Developmental Pathology and Tooth 
Decay — The Dental Cosmos, 1905. 

Errors in Dental Education — The 
Dental Cosmos, 1906. 

91. Interstitial Gingivitis due to Autoin- 

toxication: Etiology — The Dental 
Digest, 1906. 

92. Interstitial Gingivitis due to Autoin- 

toxication as Indicated by the 
Urine and Blood Pressure Diag- 
nosis — The Dental Digest, 1906. 

93. Therapeusis and Treatment of In- 

terstitial Gingivitis due to Auto- 
intoxication — The Dental Digest, 

94. Acid Autointoxication and Systemic 

Disease the Cause of Erosion and 
Abrasion — Proceedings of the 
Neiv York State Dental Society, 

95. Alcohol in its Relation to Degener- 

acy — Journal of the American 
Medical Association, 1907. 

96. Acid Intoxication or Acidosis: A 

Factor in Disease — Neiv York 
Medical Record, 1907. 

97. Stomatology in its Medical Aspects 

— Extrait du Bulletin of the Inter- 
national Association of Stomatol- 
ogy, Bruges, 1908. 

98. Swan Songs and Degeneration of 

American Dental Colleges — The 
Dental Cosmos, 1908. 

99. The Care of the Teeth — Illinois 

Medical Bulletin, 1908. 

100. Etiology of Face, Nose, Jaw and 

Tooth Deformities — Journal of 
the American Medical Associa- 
tion, 1909. 

101. Bone Pathology and Tooth Move- 

ment — Journal of the American 
Medical Association, 1909. 

102. Acidosis, Indicanuria, Internal and 

External Secretions: the Effects 
upon the Alveolar Process and 
Teeth — The Dental Cosmos, 1908. 

103. Sense and Nonsense as taught in 

American Dental Schools — The 
Dental Cosmos, 1909. 

104. Treatment of Interstitial Gingivitis 

— The Dental Cosmos, 1909. 

105. Progress of Stomatology in Europe — 

The Dental Cosmos, 1909. 

106. Hard Teeth and Soft Teeth— The 

Dental Cosmos, 1909. 

107. Progress of Stomatology in Hungary 

— American Journal of Clinical 
Medicine, 1909. 

108. Local Manifestations of Systemic 

Diseases — XVI International Med- 
ical Congress, Budapest, 1909. 

109. How Shall the Stomatologist be Edu- 

cated ? — International Association 
of Stomatology, Budapest, 1909. 

no. Scope of Developmental Pathology 
— The Alienist and Neurologist, 
Feb. 1910. 

in. Rip Van Winkles in American Dent- 
al College Faculties — The Dental 
Cosmos, 1910. 



The Scope of Developmental Pathol- 
ogy in its Relation to Oral Mani- 
festations — International Ameri- 
can Congress of Medicine and 
Hygiene, 1910. 

Oral Hygiene in American Dental 
Schools — The Dental Cosmos, 

The Acidemic Condition — The Med- 
ical Standard, 1910. 

Iodin as an Astringent, Antiseptic, 
Disinfectant and Germicide in the 
Treatment of Mouth Diseases — 
Journal American Medical Asso- 
ciation, 1910. 

How Shall the Stomatologist be Ed- 
ucated? — Journal American Med- 
ical Association, 1910. 

Care of the Mouths of School Chil- 
dren — The Dental Summary, 

The Quality of Service Rendered — 
The Dental Summary, 1910. 

What are Dentists as a Profession 
doing to Advance their Specialty? 
— The Dental Summary, 1910. 

Treatment to Alleviate the Conta- 
gions, Infections and Local Dis- 
eases of School Children — The 
Dietetic and Hygienic Gazette, 

Developmental Pathology: A Study 
in Degenerative Evolution — Pro- 
ceedings of the First District 
Dental Society of Neiu York, 

The Future of Dentistry — Sunday 
Editorial in The Chicago Tribune 

Some Bacterial and Non-Bacteriai 
Diseases — Dental Summary, June 

The Relation of Rheumatic Arthri- 
tis to Pyorrhoea Alveolaris — 
Clinical Medicine, November , 

Degeneracies, the Result of Alcohol 
and other Narcotics — Read before 
Society for the Study of Alcohol 
and Other Narcotics, at Washing- 
ton, D. C, Dec. 11-12, 1912. 

Interstitial Gingivitis and Pyorrhoea 
Alveolaris — Journal American 
Medical Association, 1913. 



Adami 123 

Alexander, H. C. B 173 

Allbright 3 

Allen, Harrison 22 

Andrews. R. R 88 

Arkovy 4 

Atkinson 4 

Barker 272 

Barrett 314 

Bauman 239 

Beaumont 203 

Bernard, Claude 203 

Bichat 201 

Biehn, J. Favil 328 

Billings, Frank 298 

Bla ck 5, 42, 50, 52, 53, 56, 57 

Boak, G. D 213 

Boedecker 314 

Bondurant 207 

Bonwill 2 

Bouchard, H. H 184, 239 

Braconnot 239 

Bremer, L 228 

B ro wn 2 

Brown-Sequard 271 

Brubaker, A. B 90 

Bui lard 227 

Calve, Marshall 2 

Carpenter 104, 108, 109, 283, 289 

Carter 239 

Cartwright, Hamilton 4 

Chittenden, Prof. Russell H 242 

Christian 202 

Clowes 3 

Coles, Oakley 4 

Collins, J 86 

Congdon, Ernst 90 

Coplans, Mayer 219, 220 

Croftan, Alfred C 70 

Cruveillier 207 

Davis, David J 308 

Dickinson, Howship 78 

Dray, Arthur R 21 

Ebner, Von 62 

Eisenhart 277 

Enderlein 76 

Essig, C. J 3 

Evans, W. A 106 

Farrar, J. N 4 

Fauchard, H. A 2 

Fitzgerald, John 10, 90, 295, 296 

Flower, Alsop E 126 

Foster 14 

Gallippe 4, 16, 104 

Geddings, H. D 75 

Gilmer 305 


Gmelin 239 

Goadby, K. B 220, 302 

Gubler 239 

Hafner 215 

Hammarsten 87 

Hartzell, T. B 306 

Hassal .239 

Head, Joseph 325 

Hektoen 156, 265 

Herschell 296 

Hertwig 62 

Herzog 108 

Hodgen 233 

Hogben 173 

Howell 177 

Hunter 298, 301 

Ingersoll, L. C 4 

Izklai, Joseph 4 

Jacobson 75 

Jaffe 239 

Joirac, M 2 

Jourdain 2 

Jurgensen 194 

Kaecker, L 2 

Kaufmann 66, 275, 276 

Kiernan 271 

Kirk 124, 184, 206 

Klebs 122 

Koch 16 

Kolliker 35, 37, 62, 279 

Krabler 194 

Kuh, Sidney 273 

Kuttner 282 

Libman, E 309 

Macauley 242 

Magitot 2, 8, 57, 61, 64, 206 

Mailhol 14 

Malassez 4 

Malenfant 79 

Marinesco 271 

Mendel 228 

Metchnikoff 236, 239, 258 

Miller 9, 102, 103, 104, 105, 286 

Mills, G. A 3 

Minot 38, 58, 62 

Moorehead, Frederick 299 

Morgan, de 36 

Moyer 233 

Mummery 21 

Murchison 202 

Murrell 228 

Nasse 271 

Nencki 239 

Niles, N. S 3 

O'Neill, Eugene F 21 

Osier 300 




Parker 213 

Patterson, J. D 4, 6, 9, 103 

Pedley, Newland 7, 8 

Pierce, C. N 9, 16, 90, 91, 206 

Pitres 273 

Planer 238, 239 

Prout 203 

Purdy 257 

Quain 13 

Rawls, A. 4, 233 

Recklinghausen, von 277 

Reese 4 

Reeves 90 

Rehwinkle 3 

Rennert 232 

Rhein, M. L 9, 90, 104, 105, 206, 314 

R 'g» s > John T 2 

Robin 57, 60, 61, 64, 206, 239 

Roger, G. H 239 

Rokitansky 282 

Rosenow, Edward E 309 

Rush 228 

Salisbury, J. H 79, 91, 93 

Salkowsky 239 

Salter 52 

Sayre, Charles E 126 

Scheele 87, 89 

Scheff 2 

Scheheotskey 78 

Schieff 239 

Schmidt 78 

Selmi 235 

Senator 239 

Shambaugh, G. E 299 


Sirletti 3 

Stadeler 239 

Starr, A. R 5 

Stevenson 78 

Stewart 297 

Suckdorf 237 

Sudduth, W. X 6, 8, 9, 105, 279 

Sutton, Bland 8 

Talbot, E. S 5, 10, 11, 12, 104, 182 

186, 191, 197, 324 

Thoma 122 

Thompson 202 

Tiedemann 239 

Tomes 36, 314 

Tuke 203 

Turck 272 

Vaillard 273 

Valentine 271 

Vaughn 195 

Vignas 237 

Virchow 282 

Waldeyer 62 

Walker 4, 21 

Waller 271 

Ward, Charles 22 

Wesener 91, 92 

Whitney, J. M 326 

Whitslar, W. H 316 

Wood, James 227 

Wright, A. E 219 

Zawadsky 76 

Ziegler 32, 212, 276 

Ziemssen 194 

Zilz 300 


Abscess, Alveolar, 290. 
Alveolar, Production of, 290. 
Formation, Description of, 117. 
Pericemental, 297. 
Peridental, 123. 
Abscesses, Location of, 287. 

Treatment of, 326. 
Acid Autointoxication and Mouth Acidity, 

Excess of System, Disposal of, Through 

Salivary Glands, 254. 
States, 198. 
Alcohol, Constitutional Effects of, 226. 

Effect of, on Alveolar Process, 224. 
Altitude, High, Effect of, on Alveolar 

process, 216. 
High, Effect of on Teeth and Gums, 215. 
Alveolar Abscess, 290. 

Production of, 290. 
Alveolar-Process, abnormal, 30. 
Absorption of, 25, 28, 121, 189, 205, 271, 

Absorption of, and Calcic Deposits on 

Roots of Teeth, 275. 
Absorption of, Caused by Excessive 

Brushing of Teeth, 189. 
Absorption of, in Asthma, 205. 
Absorption of, in Bright's Disease, 205. 
Action of Poisons on, 223. 
And High Blood Pressure, 208. 
And Lessened Blood Alkalinity, 256. 
And Poisons in Circulation, 209. 
Arrested Development of, 30. 
As End Organ, 70, 118, 121, 236. 
As Transitory Structure, 236. 
Atrophy of, 197. 
Blood Vessels of, 177. 
Changes in Function of, 184. 
Effect of Acid States on, 199. 
Effect of Constitutional Disturbances on, 

Effect of Diabetes on, 207. 
Effect of Exanthemata on, 205. 
Effect of High Altitude on, 216. 
Effect of Interstitial Inflammation on, in 

Dog's Tooth, 137. 
Effect of Nutritional Disturbances on, 

Effect of Picking Teeth on, 190. 
Effect of Pregnancy on, 200. 
Effect of Tobacco, Alcohol, Tea, Coffee, 

Drugs and Poisons on, 224. 
Effect of Toxins on, 223. 
Endarteritis Obliterans and Arterioscle- 
rosis of Vessels in, 266. 
Exfoliation of Anterior Plate of, 326. 
Growth of, 24. 

Alveolar-Process, Hypertrophy of, 30, 33. 
In Phosphorus Poisoning, 121. 
In Tuberculous Monkey, Absorption of, 

J 55- 
Inflammations of, 113. 
Injury to, by Bridgework, 188. 
Injury to, by Gold Crowns, 188. 
Nerve Supply in, 123. 
Obliteration of Arterioles in, 266. 
Osteomalacia of, 197, 200, 277. 
Overlapping Fillings Cause of Injury to, 

Structure of, 25. 
Toxemia and, 199. 
Transitory Nature of, 69, 96. 
Under the Microscope, 35. 
Wasting of, and Facial Hemiatrophy, 
Antimony as Cause of Interstitial Gin- 
givitis, 173. 
Arsenic as Cause of Interstitial Gingi- 
vitis, 173. 
Arteries, Changes in Walls of, in Disease, 
Irritations of Walls of, 263. 
Arteriosclerosis and Nerve End Oblitera- 
tion, Degeneration, 261. 
Of Alveolar Blood Vessels, 266. 
Asthma, Absorption of Alveolar Process 

in, 205. 
Atmospheric Pressure and Bleeding From 

Gums, 215. 
Atrophy from Disuse, 237. 
Autoinfections, 236. 
Autointoxication, 236, 244. 
Factors in, 201. 
In Interstitial Gingivitis, 235. 
In Neurotics and Degenerates, 242. 
Indicanuria as Source of, 258. 
Urinary Signs of, 247. 
Bacillus Coli Communis as Inhabitant of 

Mouth, 296. 
Bacteria Infesting Mouth, 296. 
Bacterial Experiments in Interstitial Gin- 
givitis, 104. 
Infection of Man, 236. 
Thrombosis in Peridental Membrane, 
Bacteriology of Interstitial Gingivitis, 104. 
Bile, Composition of, 75. 
Blood, Alkalinity Effect of Lessened, 256. 
Analysis of, 73. 

From Portal Vein, Toxicity of, 240. 
Pressure, High, and Alveolar Process, 

Pressure, High, and Gingivitis, 208. 



Blood, Vessels of Gums Alveolar Process 

and Pericemental Membrane, 177. 
Body Equilibrium, Maintenance of, on Re- 
stricted Diet, 242. 
Heat, 196. 

Refrigeration of, 212. 
Temperature and Climate, 211. 
Bone Absorption, 66. 

Absorption in Inflammation, 120, 124. 
Building and Absorption, 64. 
Brass-Worker's Ague as Cause of Inter- 
stitial Gingivitis, 172. 
Bridgework, Injurious Effect of, on Aveo- 

lar Process, 188. 
Bright's Disease, Absorption of Aveolar 

Process in, 205. 
Bromides as Cause of Interstitial Gingivi- 
tis^ 173. 
Cachexia, 198. 

Calcic Deposit: See also Tartar. 
Calcic Deposits on Teeth: See also Serum- 

al Deposits. 
Calcic Deposits on Teeth, io, 83, 280. 

Deposits, Removal of, 323. 
Calcification, Causes of, 282. 
Calcospherites, 50, 162. 
Catarrh Coexistent with Pyorrhoea Alveo- 

laris, 103. 
Cementoblasts in Dog's Tooth, ij.g. 
Children, Neurotic and Degenerate, Erup- 
tion of Teeth in, 182. 
Climate and Scurvy, 218. 
Coca, Abuse of, 229. 
Cocain, Effect of, on Gums, 230. 

Effects of Use of, 229. 
Coffee, Nervous Symptoms of, 22-. 
Criminals, Chest Formation of, 205. 

Tuberculosis in, 205. 
Crowns and Bands, 320. 
Degeneracy of Tissues, 100. 
Degenerates, Autointoxication in, 242. 
Dental Arches, Irregular, 102. 
Pulp: See also Tooth. 
Pulp, 118. 

Shelf, Development of, 58- 
Shelf, Embryology of, 62. 
Dentistry as Cause of Interstitial Gingivi- 
tis, '182. 
Modern, Diseases Caused by, 319. 
Dentures, Artificial, 320. 
Digestive-Apparatus, Evolution of, 237, 
In Differing Types, 241. 
Diabetes, Effect of, on Alveolar Process, 

207. _ 
Diabetic Patients, Uranalysis in, 251. 
Drug Poisons, Nervous Effects of, 231. 
Drugs, Effect of, on Alveolar Process, 224. 
Nervous Symptoms Due to Use of, 228, 

Poisonous Effects, First Noted in Gums, 
230, 234. 
Dyphodontia, 12. 

Emotions and Their Physical Effects, 201. 
And Trophoneuroses, 271. 
Violent, and Nutrition, 204. 

Enamel Organ, 59. 
Endarteritis, Causes of, 263. 

Definition of, 263. 

Obliterans and Nerve End Degenera- 
tion, 261. 

Obliterans in Alveolar Blood Vessels, 
Environment in Interstitial Gingivitis, 95. 
Epithelial Debris, 60. 
Evolution of Digestive Apparatus, 237, 

Exanthemata, Effect of, on Alveolar 

Process, 205. 
Face, Evolution of, 113. 
Facial Hemiatrophy and Wasting of 

Alveolus, 208. 
Faeces, Salts in, 76. 
Fever, Cause of, 195. 
Fever, Definition of, 194. 
Fevers, Trophic Changes After, 206. 
Gum Margin, Irritation of, 182. 

Massage, 314, 316. 

Wash, 316. 
Gums, Bleeding From as Effect of At- 
mospheric Pressure, 215. 

Bloodvessels of, 177. 

Effect of High Altitude on, 215. 

Effect of Poisons on, 199, 230. 

First Structure to Indicate Certain Sys- 
tematic Defects, 250. 

Inflammation of, in Scurvy, 209, 220. 

Irritation of, 66. 

Signs of Drug and Metal Poisoning in, 

Structure of, 40. 

Ulceration of, 271. 
Gingival Glands, 52. 

Organs, 52, 90. 
Gingivitis, Philology of, 14. 
Gold Crowns and Destruction of Alveolar 

Process, 188. 
Gout, Deposits in Tissues in, 79. 
Halisteresis, Definition of, 276. 
Heat, Difference Between that of Sun and 

Shade Heat, 213. 
Heredity in Interstitial Gingivitis, 95, 96. 
Horses, Cause of "Cribbing" in, 126. 
Hygiene in the Tropics, 213. 
Hypophysis Cerebi, Disorders of, and Body 

Changes, 34. 
Indican, Effects of Administration of, 239. 

In Organism, Effect of, 258. 
Indicanuria and Neurasthenia, Relation 
ship of, 257. 

As Source of Autointoxication, 258. 
Infection, Susceptibility to, and Low Tern 

perature, 212. 
Inflammation, Active, Illustration of, 114 

And Bone Absorption, 120. 

Behavior of Blood in, 115, 120. 

Leucocytes in, 115. 

Nervous System in, 122. 

Production and Course of, 114. 

Without Gingivitis, 112. 
Iodoglycerole, 318. 
Insane, Disturbances of Teeth in, 207. 



Instruments to be Used in Removing Cal- 
cic Deposits, 323. 
Intermarriage, Effect of, on Teeth, 97. 
Interstitial, Foster's Definition of, 14. 

Quain's Definition of, 13. 
Interstitial-Gingivitis and Constitutional 
Diseases, 236. 

And High Blood Pressure, 208. 

And Inorganic Salts, 73. 

And Irregular Arches, 102. 

And Uric Acid, 87. 

And Pericementitis, 176. 

And Poisons in Circulation, 209. 

Animal Research on, 125. 

Antimony as Cause of, 173. 

Arsenic as Cause of, 173. 

Autointoxication in, 235. 

Bacteriologic Researches in, 104. 

Brass-worker's Ague as Cause of, 172. 

Bromides as Cause of, 173. 

Contagiousness of, 6. 

Caused by Regulation of Teeth, 190. 

Choice of, in Preference to Pyorrhoea 
Alveolaris, 13, 15. 

Condition of Urine in, 247. 

Constitutional Causes of, 8, 84, 194, 327. 

Definition of, 112. 

Degenerate Tissues in, 100. 

Differential Diagnosis of, 221. 

In Defective Children, 103. 

In Dogs, 126. 

In Dogs, Technique of Examination for, 

In Human, Autopsy Findings, 156. 

In Man From Drugs, 170. 

In Pregnant Women, 8, 176. 

In Soldiers in the Tropics, 213. 

Infectivity of, 17. 

Influence of Climate in, 211. 

Iodin Treatment of, 317, 322. 

Irregular Teeth and, 6. 

Laboratory Experiments in. 105. 

Local and Constitutional Causes of, 104, 

Local Causes of, 5, 84, 104, 112, 175, 182. 

Mercurial, in Dogs, 150. 

Method of Extension of, to Aleovolar 
Process, 276. 

Drug and Metal Poisons in Etiology of, 

Etiology of, 84. 

Frequency of, in Animals, 126. 

Heredity and Environment in, 95. 

History of, 1. 

In Animals, 7, 8. 

In Children, 82. 

Modern Dentistry as Cause of, 182, 186. 

Nature of Structures Involved in, 112. 

Pathognomonic Symptoms of, 312. 

Persons with Predisposition to, 124. 

Point of Commencement of, 56. 

Predisposition to, 100. 

Pregnancy and, 8, 176. 

Recovery From, 286. 

In the Human, Researches on, 156. 

Scorbutus in, 85. 

Interstitial-Gingivitis, Scurvy in, 218. 

Symptoms of, 7. 

Syphilis in, Etiology of, 8, 9. 

Tartar as Cause of, 112. 

Theories of, 84. 

Tooth Eruption and, 182. 

Treatment of, 310. 

Trophic Disturbances in, 86. 

Uncleanliness as Cause of, 186. 

Vaccine Treatment of, 328. 

With Intestinal Fermentation, 244. 
Intestinal Putrefaction and Toxins in the 

Blood, 239. 
Jaw, Arrested Development of, 95. 

Effect of Phosphorus Poisoning on, 120. 

Excessive Development of, 95. 

Variation in Dogs, 127. 
Jaws, changes in, 238. 

Deformities of, 242. 

Evolution of, 19, 113. 

Irregular in Neurotics and Degenerates, 
Kidney Disease, Absorption of Alveolar 

Process in, 205. 
Laboratory Experiments in Interstitial 

Gingivitis, 105. 
Lymph, Salts in, 76. 

Mallet, Excessive Use of as Cause of In- 
flammation of Peridental Membrane, 
Maxillary Necrosis, 271. 
Metabolic Disturbances and Their Effects, 

Mental States, Physical Effects of, 201. 
Mouth Acidity and Acid Autointoxication, 

Infection and Glandular Affections, 297. 

Toxins Generated in, 199. 
Mucous-Membrane, Glands, in, 50, 57. 

Irritation of, 66. 

Of Mouth, 38. 

Of Mouth, Blood Vessels and Nerves of, 

Under Microscope, 53. 
Nerve End Degeneration, Endarteritis, 
and Arteriosclerosis, 261. 

Exhaustion in Parents, Effect of, on 
Child's Teeth, 97, 101. 

Supply in Alveolar Process, 123. 
Nerves, Effects of Toxins on, 273. 
Nervous System in Inflammation, 122. 
Neurasthenia and Indicanuria, Relation- 
ship of, 257. 
Neurotics, Autointoxication in, 242. 
Nutrition, Causes of Arrest of, 223. 

Disturbances of, Effect of, on Alveolar 
Process, 223. 

Modification of, by Emotions, 204. 
Opium, Nerve Effects of, 228. 
Osteoclasts, 279. 
Osteomalacia, 197. 

Of Alveolar Process, 197, 200, 277. 

Varieties of, 276. 
Pancreatic Juice, Composition of, 76. 
Paretic Patients, Urine in, 252. 



Pericemental Membrane, Bloood Vessels 

of, 177. 
Pericementitis, 175. 

And Interstitial Gingivitis, 176. 

Artificial Production of, 176. 

Author's Researches on, 176, 178. 

Causes of, 176. 

Due to Syphilis, 176. 

Effect of on Surrounding Tissues, 176. 

In Human, Research on, 175. 

Phagedenic, 53. 
Peridental Abscess, 123. 
Peridental-Membrane, 27, 42, 45. 

Bacterial Thrombosis in, 162. 

Blood Vessels in, 49. 

Cells in, 65. 

Condition of, in Pyorrhoea, 289. 

Cross Sections of, 57. 
Peridental-Membrane, Degeneration of, 
From Drugs, 172. 

Effect of Interstitial Inflammation on, in 
Dog's Tooth, 137. 

Excessive Use of Mallet Cause of In- 
flammation of, 187. 

Glands in, 50. 

Hard Bodies in, 50. 

Infection of, 96. 

Irritation of, 66. 
Periostitis, Suppurative, 162. 
Periosteum, 42. 

Perspiration, Inorganic Salts in, 76. 
Phosphorus Poisoning, Effect of, on Jaws, 

Poison, Scant Elimination of, by Skin, 242. 
Poisons, Action of, on Alveolar Process, 

Classification of, 223. 

Effect of, on Gums, 230. 

Elimination of, 243. 
Polyphyodontia, 12. 

Potassium Bromide as Cause of Intersti- 
tial Gingivitis, 173. 
Pregnancy, Elimination of Poisons in, 243. 

Urinary Acidity in, 244. 
Purin bodies, 88. 
Pyorrhoea-alveolaris, 96, 124, 285. 

And Irregular Arches, 102. 

Bacteria in, 106. 

Catarrh Coexistent With, 103. 

Constitutional Effects of, 295. 

Description of, 285. 

Development of, 285. 

In Animals, 106, 129, 131. 

In Dog's Teeth, Technique of Examina- 
tion for, 131. 

In the Human, 106. 

In Troops, 220. 
Rachitis, Association of, With Scurvy, 218. 
Saliva, Composition of, 78. 
Salivary Calculi, Composition of, 79. 

Concretions, 98. 

Glands, Effect of Tobacco on, 225. 
Salivation in Scurvy, 221. 
Scalers, Description of Author's, 321. 
Scurvy and Armies, 218. 

And Climate, 218. 

Scurvy, and Food, 219. 

And Inflammation of Gums, 209. 

And Interstitial Gingivitis, 236. 

Causes of, 218. 

Differential Diagnosis of, 220. 

In Interstitial Gingivitis, 218. 

In Institutions, 221. 

Rachitis with, 218. 

Salivation in, 221. 

Symptoms of, 220. 
Sedentary Habits, Effects of, 89. 
Serumal Deposits: See also Calcic De- 
Serumal Deposits on Teeth, Analysis of, 

. 79 ' 
Skin, Scant Elimination of Poisons by, 242. 
Status Epilepticus, 201. 
Submaxillary Gland, 185. 
Submucous Membrane, Proliferation of 

Epithelial Cells in, 58. 
Syphilis and Interstitial Gingivitis, 236. 
Tabes Dorsalis, Urine in, 252. 
Tartar: See also Calcic Deposit. 
Tartar, 184, 320. 

And Malnutrition, 185. 
Salivary, Formation of, 184. 
Solvent For, 325. 
Tea-tasters, Nervous Symptoms in, 226. 
Teeth: See also Tooth. 
Teeth, Calcic Deposits on, 280, 323. 

Cavities in, and Overlapping Fillings, 
Cause of Injury to Alveolar Process, 
Change of Position of, 31. 
Effect of Acid States on, 199. 
Effect of High Altitude on, 215. 
Eruption of, 64, 319. 
Eruption of, and Interstitial Gingivitis, 

Eruption of, in Neurotic and Degenerate 

Children, 182. 
Evolution of, 113. 

Examination of, for Uric Acid, 90. 
Excessive Brushing of, and Bone Ab- 
sorption, 189. 
Decay of, 196. 
Deformities of, 242. 

Degeneration of, Due to Evolution, 238. 
Devitalization of Pulps of, 188. 
Disturbances of, in the Insane, 207. 
Falling Out of, and Trophoneuroses, 

Description of, 285. 
Individual, Correction of, 320. 
In Inmates of Institutions, 221. 
Irregular, 186. 
Loosening of, 271. 
Method of Eruption of, 64. 
Milk, Formation of Papilla; for, 58. 
Of Defective Children, 103. 
Picking of, Effect of, on Alveolar Pro- 
cess, 190. 
Proper Way of Brushing, 313. 
Result of Wedging Apart of, 193. 
Regulation of, and Interstitial Gingivi- 
tis, 190. 



Teeth, Shape of Crowns of, 27, 29. 

Sockets of, 26. 
Temperature, Sudden Changes in, Consti- 
tutional Effects of, 215. 

Effect of Lowering of, 21 r. 
Tissue Degeneration in Internal Organs, 

Tobacco, Constitutional Effects of, 224. 

Effect of, on Alveolar Process, 224. 

Effect of, on Salivary Glands, 225. 

Mental Effects of, 225. 
Tooth: See also Teeth. 
Tooth Brush, Best Kind to Use, 313. 

Destruction, Role of Friction of Lips, 
Teeth and Foreign Bodies in, 250. 

Germs, Development of, in Mammals, 

Pulp, Death of, 196. 
Toxins, Effect of, on Alveolar Process, 

Toxins Producing Trophic Changes, 223. 
Transitory-Structures, 19, 24. 

Arrested Development of, 113. 
Trophic Changes Caused by Toxins, 223. 
Trophoneuroses and Emotions, 271. 

Tropics, Hygiene in, 213. 
Tuberculosis and Interstitial Gingivitis, 

Effect of, on Alveolar Process, 207. 

In Criminals, 205. 
Ulceration, Location of, 289. 
Uric-Acid and Interstitial Gingivitis, 87. 

Crystals on Teeth, Inaccuracy of Dry 
Distillation Test for, 92. 

Laboratory Examination of Teeth for, 

Poisoning, 89. 

Tests for, on Teeth, 90, 91. 
Urinary-Acidity in Pregnancy, 244. 

In Senility, 255. 

In various diseases, 254. 
Urine, Examination of, in Interstitial Gin- 
givitis, 247 

In Diabetic Patients, 251. 

Inorganic Salts in, 77. 

In Paretic Patients, 252. 

In Tabetic Patients, 252. 

Report of 394 Examinations, 247. 

Toxins in, 201. 
Wallerian Degeneration, 271.